PHYSIOLOGY OF BLOOD

Lecture 1
Theme: Blood composition, amount and properties.
Plan: 1. Concept of blood system.
2. Blood basic functions.
3. Blood composition and amount (hypervolemia, hypovolemia).
4. Blood plasma.
5. Physical and chemical properties of blood (osmotic pressure, oncotic pressure,
viscosity, relative density).
6. Buffer systems of blood.
1. Concept of blood system

Blood along with interstitial fluid and lymph is an important component of

the internal environment of an organism, the relative constancy of which, including
physical and chemical parameters (рН, osmotic pressure, temperature, etc.), is a
necessary condition of vital activity of an organism. Changes of physical and
chemical properties of blood, which are the important mechanism in pathogenesis
of many diseases, are used for their diagnostics, assessment of the efficacy of
treatment and prognosis.
System of blood, as proposed by G.F. Lang (1939), includes:
1. Blood (in vessels).
2. Organs of haemopoiesis — red bone marrow, lymph nodes, spleen,
thymus gland.
3. Organs of blood destruction (liver, bone marrow, spleen).
4. Neurohumoral apparatus.
The main place of blood cells formation is the red bone marrow. Here, also
the destruction of cells (erythrocytes), re-using of iron, synthesis of Hb, and
maturing of B-lymphocytes populations — factors of humoral immunity, takes
place.
In thymus gland, the formation of T-lymphocytes takes place. Besides, the
spleen, lymph nodes and other lymphoid formations (Peyer's plaques, tonsil,
appendix, etc.) take part in the development of immune components.
Lymphocytopoiesis, Ig synthesis, destruction of erythrocytes, leucocytes,
thrombocytes, deposition of blood is carried out in spleen.

2. Blood basic functions

 1. Transport (transition of various substances).
2. Respiratory (transition of oxygen from respiratory organs to tissues, and
СО2 in reverse direction).
3. Trophic or nutritional (transition of nutrients from digestive duct to cells
of an organism and use of blood components by cells of tissues and organs for
plastic and energy needs).
4. Excretory (transition of waste and harmful substances to excretory
organs: products of metabolism, excessive mineral and organic substances formed
during metabolism or coming with food).
5. Temperature control (blood is warmed up in internal organs where a lot of
energy is formed, and is cooled down at upper layers of the organism.
6. Homeostatic (along with interstitial fluid and lymph it forms the internal
environment and participates in maintenance of its constancy).
7. Provides water-salt exchange between blood and tissues.
8. Protective (contains factors of humoral and cellular immunity: antibodies,
phagocytes, factors of coagulation, interferon, populations Т- and B-lymphocyte,
etc.).
9. Correlative (blood transfers biologically active substances which provide
interconnection between various organs and tissues thus ensuring the organism to
function as a whole).
10. Maintenance of the constancy of base-alkaline state due to buffer system.

3. Blood composition and amount

Blood consists of plasma and uniform elements (erythrocytes, thrombocytes,

leucocytes).
Between the volume of plasma and uniform elements there is a certain
interrelation which is called hematocrit number. Hematocrit is a part of the volume
of blood for the part of cells. In norm, the volume of erythrocytes in men
compounds 44–46%, plasma 54–56%. To transform it into SU (system of units)
the obtained number is multiplied by 0,01. It is in norm: in men 0,44–0,46, in
women 0,41–0.43. In a newborn hematocrit is 10% higher.
Amount of blood. In adult the absolute amount of blood compounds
approximately 4,5–6 liters. Its relative contents corresponds to 6–8% of the body
weight (in a newborn — 15%).
The normal contents of blood is called normovolemia. There are simple,
oligocythemic and polycythemic normovolemia (tabl. 1).
Simple normovolemia — normal interrelation between the volume of
uniform elements and plasma.
Oligocythemic normovolemia — is met at anemia as result of loss of blood
when the volume of blood is restored due to fluid part as result of transition of
interstitial fluid into vessels and the amount of uniform elements was not yet
restored.
Polycythemic normovolemia — at transfusion of small amounts of
erythrocytic mass.
Increase of blood amount ( hypervolemia, plethora).
1. At administration of big amount of blood.
2. At intensive haemopoiesis (increase of erythrocytes amount).
3. At delay of water in an organism (disease of kidneys).
4. At excessive water intake.
Decrease of amount bloods (hypovolemia).
1. At acute loss of blood.
2. At anemia.
3. At loss of fluid (dehydration of an organism), for example, at profuse
diarrhea, continuous vomiting.
Table 1
Changes of blood volume

Interrelation between uniform Variant of volemia Hematocrit number

elements and plasma
NORMOVOLEMIA
UE 0,45% plasma 0,55% Simple normal
UE 0,35% plasma 0,65% Oligocythemic below normal
UE 0,55% plasma 0,45% Polycythemic above normal
HYPOVOLEMIA
UE 0,45% plasma 0,55% Simple normal
UE 0,35% plasma 0,65% oligocythemic below normal
UE 0,55% plasma 0,45% Polycythemic above normal
HYPERVOLEMIA
UE 0,45% plasma 0,55% Simple normal
UE 0,35% plasma 0,65% oligocythemic below normal
UE 0,55% plasma 0,45% Polycythemic above normal

Note: UE — uniform elements of blood.

Kinds of hypervolemias:
Simple — proportional increase of uniform elements and plasma (at
hemotransfusion). Hematocrit in normal.
Oligocythemic — increase of blood volume due increasing its fluid part
(administration of blood-substituting fluids, dysfunction of kidneys). Hematocrit is
lower.
 Polycythemic — increase of volume of blood due to increased amount of
uniform elements (compensatory character in mountains populations). Hematocrit
is increased.
Kinds of hypovolemia:
1. Simple — proportional decrease of volumes of uniform elements and
plasma (it is short-term at acute hemorrhages). Hematocrit is unchanged.
2. Oligocythemic — decrease of blood volume due decrease of the amount
of uniform elements after loss of blood (when the volume of blood is restored due
to coming of interstitial fluid into vessels). Hematocrit is decreased.
3. Polycythemic — decrease of blood volume due to decrease of fluid part of
blood (clotting at dehydration, for example, at profuse diarrhea, continuous
vomiting, hyperhidrosis). Hematocrit is increased.
By the degree of participation in circulation there are deposited blood (45–
50%) and circulating blood (50–55%).
Depot of blood:
Liver. Big amount of blood is deposited (up to 20% of its general volume),
but completely (opposed to spleen) is not excluded from the general blood flow.
Spleen. In the spleen up to 500 ml (10–16%) of blood can be deposited
(excluded from blood flow).
Skin. Blood is deposited in capillars and veins (about 10%). Deposition
blood in skin is connected with thermoregulation.
Lungs. Deposition of blood due to change of the volume of arteries and
veins.
Venous system (regarded as depot of fluid part of blood containing
significant amount of lymph).
Lymph in lymphatic vessels may be regarded as depot of fluid part of blood.
Transfer of the deposited blood into circulation one is observed at:
1. Emotional state.
2. Physical strain.
3. Air hunger (hypoxia).
4. Hemorrhages.
Value of depot of blood. Opportunity of fast increase of mass of the
circulating blood necessary in concrete conditions for maintenance of needs of an
organism in oxygen (at climbing up the mountains, at physical work and other
states connected with increased oxygen consumpyion).
Hemorrhages and their effects. For a healthy man a single loss of 1/3 or
even 1/4 of the volume of the circulating blood is life-hazardous (decrease of blood
pressure, hypoxia). Sudden loss of 50% of blood leads to death, slow loss (within
several days) of this amount of blood is not lethal as in these situation there is
enough time for the compensatory mechanisms directed to the stabilization of
blood pressure and elimination of hypoxia to mobilize.
 Babies and newborns are especially sensitive to hemorrhages (compensatory
mechanisms are not yet well developed). Sensitivity to hemorrhages increases at
narcosis, hypothermia, pain and shock.

4. Blood plasma

Plasma is a colloid-polymeric solution in which Н2О is a solvent, dissolved

substances are salts and low-molecular organic compounds. Colloidal component
are proteins and their complexes. Plasma - fluid part of blood (its volume is
approximately 2,8–3,0 l).
Structure of plasma: H20 (90–92%) and solid (dense) residual (8–10%)
which includes inorganic and organic substances.
I. Organic part:
Proteins (albumins, globulins, fibrinogen) — 65–80 g/l.
1. Albumins (45g/l).
 Form 80% of colloid-osmotic pressure (high concentration, relatively
small size of molecules).
 Participation in regulation of water-salt balance.
 Transport of many substances (bilirubin, fats acids, exogenous
substances, including drugs — antibiotics, sulfanilamids, mercury,
and others); ¾ Binding of hormones (for example, thyroxine).
 Protein reserve.
2. Globulins (20–35g/l) – α1 -, α2 -, ß1 – ß2 - and Y- fractions. α-globulin
— thyroxinbinding protein;
— transcobalamin (В12);
— cortisolbinding protein. ß-globulin
– transmitting agent of lipids, lipoids and polysaccharides.
— transport of Cu, Fe (transferrin). Y-globulins
— (IgA, IgD, IgE, IgG, IgM) immune functions. Agglutinins of bloods are
related to this fraction.
3. Fibrinogen (2–3 g/l) — participates in blood coagulation.
Formation of proteins:
а) Albumins, fibrinogen are formed in liver.
b) Globulins — in bone marrow, spleen, lymph nodes, cells of mononuclear
phagocytic system.
Role of plasma proteins:
 Formation oncotic pressure (1/200 of osmotic pressures of plasma).
 Maintenance of рН (buffer properties).
 Maintenance of viscosity of blood (important for blood pressure).
 Prevent sedimentation of erythrocytes (stabilization).
 Participate in blood coagulation (fibrinogen, etc.).
 Factors of immunity (immunoglobulins).
  Transport (transmission of hormones).
 Nutrient (plastic).
 Regulators of concentration of free ions, for example, Fe ++
(transferrin).
 Inhibitory in relation to some proteases (antitrypsin — inhibitor of
trypsin).
 Regulators of functions, metabolism (proteins hormones, enzymes).
 Provide redistribution of water between tissues and blood (1 g of
albumin binds 0,35 g of water and at swelling it can bind up to 18 ml
of water. At hypoproteinemia (decrease of protein up to 55 g/l) —
edemas occur. Hungry edemas, for example, at starvation.
Glucose. Concentration in adults:
 Whole blood — 3,30–5,55 millimole/l.
 Plasma — 3,88–6,10 millimole/l.
 In newborn — 1,70–4,20 millimole/l.

3. Not proteins, keeping nitrogen, substances (polypeptides, amino acids,

urea, urinary acid, creatine, creatinine, bilirubin, etc.).
Not proteins (residual) nitrogen —14,3–28,5 millimole/l.
Triglycerides — 0,40–1,81 millimole/l.
Cholesterin 3,64–6,76 millimole/l.
Also, plasma contains hormones, vitamins and enzymes.
II. Inorganic part: gases (О2, nitrogen,СО2) and mineral substances.
Mineral substances — 0,9% (ions of potassium, sodium, chlorine, calcium, НСО-
, НРО- , etc.). The basic cation of plasma are Na+ , K+ , Са++, which play an
important role in maintenance of osmotic pressure, redistribution of water between
blood and tissues, coagulation of blood, excitability and contraction of cells, etc.
The basic anions of plasma are CI- , sodium hydrogenums НСО3-, phosphates
playing an important role in the regulation of рН, acid-base state, excitability of
cells, and other.

5. Physical and chemical properties of blood

Osmotic pressure is equal to 7,6–8,1 atm. It is formed mainly by salts in the

dissociated state. The osmotic pressure has important value in maintenance of
concentration of various substances dissolved in fluids of organism, and promotes
distribution of water between blood, cells and tissues.
By size of osmotic pressure in comparison with osmotic pressure of blood
there are isotonic, hypotonic and hypertonic solutions.
Isotonic solution is the one osmotic pressure of which is equal to that of
blood (for example, 0,85% solution of NaCl). Erythrocytes placed in such solution
do not change as osmotic pressure in them and in solution is equal. This solution is
called physiological. It is used as blood-substituting solution, solvent for many
medications for parenteral administration. Over 60% of osmotic pressure of blood
is provided by NaCl. Totally, inorganic substances provide 96% of osmotic
pressure.
The hypotonic solution is a solution the osmotic pressure of which is lower
than that of blood (for example, 0,3% solution of NaCI). Erythrocytes placed in
such solution swell and burst (i.e., hemolyzed) as result of transition of water into
cells, as the osmotic pressure in erythrocyte is higher, than in solution.
The hypertonic solution is solution the osmotic pressure of which is higher
than that of blood (for example, 2% solution of NaCI). Erythrocytes placed in such
solution, wince as result of output of water from cell as the osmotic pressure in
erythrocytes is lower than in solution.
Osmotic pressure in person is rather constant. In its neurohumoral regulation
participate organs of excretion (kidneys, sweat-glands). Change of the osmotic
pressure is perceived by special osmoreceptors located both at periphery (in
endothelium of vessels) and center (in hypothalamus).
Oncotic pressure. The osmotic pressure formed by proteins is called
oncotic (due to their ability to draw Н2О).
The portion of the osmotic pressure formed by proteins is 0,03–0,04 atm.
which approximately makes 1/200 of all osmotic pressures of plasma.
Because of small size of molecules of albumins and their big amount (as
compared with fibrinogen and globulins) more than 80% of oncotic pressure are
caused by them.
Oncotic pressure is important for:
1. Formation of interstitial fluid.
2. Lymphization.
3. Formation of urine.
4. Adsorption Н2О in intestine.
5. Redistribution of Н2О between blood and tissues.
Proteins have big size of molecules and, therefore, are unable to pass
through the endothelium of capillars (remain in blood-flow). They keep certain
amount of water in blood.
Viscosity of blood: — whole — 5 (viscosity of water is accepted as 1,0);
— plasma — 1,7–2,2.
Viscosity of blood increases at dehydration of an organism which reduces
thickening (profuse diarrhea, continuous vomiting), increase in blood of uniform
elements (polycythemia, leukosis), accumulation of СО2, increased content of
proteins, especially fibrinogen. With increased viscosity of blood the
hydrodynamical peripheral resistance in vessels increases that results in difficulty
of heart work and slowing down the blood-flow.
Viscosity of blood depends on the amount of erythrocytes (tabl. 2). With the
increase of their number it rises.
 Table 2
Dependence of blood viscosity on the erythrocytes contents in it

Number of erythrocytes Viscosity of blood

4,5×1012/l 5,0
6,7×1012/ l 6,4
7,4×1012/l 8,1
9,3×1012/l 20,9

Viscosity of blood decreases at hydration of an organism (intake of great

volume of water, water delay in an organism at diseases of kidney), anemias,
hypoproteinemias, decrease of blood coagulation (under the influence of the
administered heparin). Decrease of blood viscosity leads to an acceleration of
blood-flow.
Relative density (specific gravity) of blood depends on the contents in it of
proteins, salts and erythrocytes. The relative density of the whole blood changes in
rather narrow limits (1,050–1,060), plasma 1,025–1,034, and relative density of
erythrocytes is higher than that of the whole blood and plasma (1,090).
Reaction of blood (acid-base state). Active reaction of blood (рН) is caused
by the interrelation in it of hydrogen (Н+ ) and hydroxyl (OH- ) ions. It is one of
the rigid parameters of homeostasis.
рН of arterial blood — 7,40;
рН of venous blood — 7,35 (it has more carbonic acid);
рН inside cells — 7,0–7,2 (acidic metabolic products).
рН limits compatible with life — 7,0–7,8.
But long shift of рН in 0,1–0,2 is dangerous for life. The shift of рН, first of
all, is reflected in the activity of enzymes.
Despite constant coming into blood of СО2, lactic acid and other acidic
components which can affect рН of blood, active reaction (рН) remains constant. It
is provided by buffer properties of blood and activity of excretory organs
(excretion of СО2 by lungs, excretion of acidic and holding of alkaline products by
kidney).

6. Buffer systems of blood

The buffer systems are solutions which steadily maintain the constancy of
the concentration of the hydrogen ions, both at addition of acids or alkalis, and at
dilution. They consist of mixture of weak acids with salts of these acids and strong
alkali. Due to buffer systems the active reaction of blood (рН) — the major
parameter of constancy of internal environment, is maintained.
Buffer systems of blood:
 1. Carbonate (Н2СО3+NaHCO3) and (Н2СО3+KНСО3). The acidic
components which coming into blood cooperates with bicarbonate. Alkaline
components coming into blood cooperate with Н2СО3 thus forming salt and Н2О
(removed by excretory organs).
2. Phosphate (NаН2РО4+Nа2НРО4) NаН2РО4 has the property of an acid
and reacts with alkaline components, and Nа2НРО4 — properties of alkalinity and
reacts with acid components.
3. Protein. It is caused by amphoteric properties of plasma proteins. In
acidic medium they behave like alkali, in alkaline — as acids, connectng in the
first case acids, in the second-alkalis.
4. Hemoglobin (the most powerful). The restored Нb is a weaker acid than
Н2СО3 and gives the K+ ion to it, attaches Н+ itself and becomes low-dissociated
acid.
Buffer systems are available also in tissues (the main ones are protein and
phosphatic).
During metabolism acidic products are formed more than basic, therefore the
danger of рН shift to the acidic side exists. In a human organism daily the total
acidity of НCl, lactic, pyruvic, coal, and other acids is equal to 20 – to 30 liters of
1,0 normality of НСl. Despite of it, the organism lives and the constant рН is
maintained. Buffer systems of blood and tissues provide the big steadiness to
action of acids. So, for рН shift:
to the alkaline side — it is necessary to add alkalis in 40–70 times more
than to the same amount of water;
to the acidic side — it is necessary to add acids in 327 times more than to
the same amount of water.
The alkaline salts of weak acids kept in blood, form alkaline reserve of
blood.
Shifts of active reaction of blood either to acidic (acidosis) and to alkaline
(alkalosis) sides are possible.
By the degree of intensity there are acidosis compensated and not
compensated.
In compensated acidosis at acids supply into blood the changes of the latter
can be limited only to decrease of alkaline reserve without changes of рН. Despite
chemical and functional shifts in an organism, pH is maintained at the action of
buffer systems. At exhaustion of the alkaline reserve and failure of protective
mechanisms рН is shifted outside the limits and the compensated acidosis is
developed.
By their origin there are:
1. Gaseous acidosis and gas alkalosis;
2. Nongaseous acidosis and not gas alkalosis.
Gaseous acidosis (respiratory) — at increase of H2CO3 in an organism. It
can arise at:
 1. Insufficient function of external respiration.
2. Circulatory insufficiency.
3. Inhalation of air (admixture) with the increased concentration of H2CO3.
Gas alkalosis (respiratory) — at lungs hyperventilation СО2 is excreted in
excess (mountain disease, excessive artificial respiration).
Non-gaseous acidosis (metabolic) — at accumulation in an organism of
acidic products. Such condition can arise at:
1. Excessive formation of acidic products at dysbolism (diabetes, starvation).
2. Affected excretion of acidic products from an organism (nephrites).
3. Losses of the alkali by an organism (profuse diarrhea, fistulas of
intestine).
4. Excessive administration of mineral substances into an organism
(poisoning by acetic acid).
Not gas alkalosis (metabolic) — at accumulation of alkaline products in an
organism.
Such state can arise at:
1. Administration of big amount of alkaline products into an organism
(baking soda, alkaline waters abuse).
2. Loss of big amount of gastric juice (continuous vomiting, stomachal
fistula).
3. Hyperproduction of glucocorticoids or treatment by the preparations of
adrenal hormones.

Lecture 2

Theme: Blood forming components

Plan:
1. Erythrocytes, their structure, properties and functions.
2. Hemoglobin, their structure, properties, varieties, compounds and
functions.
3. Hemolysis and its varieties.
4. Erythrocyte sedimentation rate.
5. Leucocytes, their classification, features and functions.
6. The leucocytary formula. Changes in the quantities of leucocytes.
7. Thrombocytes, their structure, properties and functions.

1. Erythrocytes, their structure, properties and functions

 Erytrological system — the physiological system including erythrocytes
circulating in blood, bodies of their formation and destruction, incorporated into
system of neuroendocrinology regulation.
In human and mammal, erythrocytes do not contain nucleus. Absence of
nucleus presumes that erythrocytes consume oxygen for own needs in 200 times
less than nuclear representatives (erythroblasts, normoblastes).
Sizes of erythrocyte: diameter — 7,7 microns, thickness — 2,2 microns.
One and important feature of erythrocytes is their form of biconcave disk.
The biconcave form erythrocytes:
 Increases in 20% common surface in comparison with the form of a
sphere.
 Performs of one of the basic functions — transition of О2 and СО2.
 Increases ability to convertible deformations (plasticity) at passage
through the narrow and bent capillaries.
At some kinds of pathologies (anemia) there are erythrocytes of various
form (crescent, pear-shaped, etc.), named poikilocytosis, and also of various size
— аnisocytosis.
By structure, erythrocyte consists of skeleton of cell — stroma, and upper
layer — membrane. Thickness of the membrane is 10 nanometers.
The membrane of erythrocyte consists of 4 layers:
 External which is formed glycoprotein.
 Average 2 layers — bi-lipid layer.
 Internal layer-protein layer.
Chemical compound of erythrocytes: 60% — Н2О, 40% — the dry
sediment (almost 90% of it is hemoglobin (Hb)).
Functions of erythrocytes:
 Transition of О2 (participation of hemoglobin).
 Transition of СО2 (participation of hemoglobin).
 Protective (absorption of harmful substances, production of antibiotic-
eritrin).
 Regulation of water-and-salt exchange.
 Transition of nutrients.
 Participation in regulation of erythrogenesis.
 Creative. It presumes transition of macromolecules ensuring
information links of the organism (see «Main Functions of Blood»).
 Participation in regulation of the acidic-basic condition (hemoglobin
buffer).
 Participation in blood coagulation (contain thromboplastin released at
their destruction. Presence of destroyed erythrocytes in blood induces
hypercoagulation and thrombus formation. Along with it, they are
heparin bearers which is an anti-coagulant).
Amount of erythrocytes in blood:
 in men — 4,5–5,0 × 1012/l ;
in women — 3,8–4,5 × 1012/l.
Increase of erythrocytes number (erytrocytosis).
Reduction of erythrocytes number (erythropenia). Erythropenia is marked at
anemia (the combination to low Hb maintenance).
Life period of erythrocytes is 130 days.
Formation of erythrocytes occurs in red bone marrow (in 1 minute it is
formed 160 × 106 of cells), and destruction — in spleen, liver, red bone marrow.

2. Hemoglobin, its structure, behavior, varieties, compounds and

functions

One of the major functions of blood is transmission of oxygen to organs and

tissues and transport of carbonic gas (CO2).
The important role in this process is played by erythrocytes due to the
presence in them of red blood pigment — hemoglobin.
Localization advantages of Нb in erythrocyte:
 Provides decrease of viscosity of blood.
 Reduces oncotic pressure, preventing loss of water by tissues.
 Prevents of Hb loss at filtration of blood in nephrones.
By the chemical nature — it is a chromoproteid consisting of protein globin
(96%) and prosthetic group of heme (4%). There are 4 groups of heme. It
represents protoporphyrin, Heme contains 4 groups. It is a protoporphyrin with a
Fe++ ion in the centre.
The key role in Hb activity is played with ion Fe++.
Functions of hemoglobin:
 Transport of О2 — oxyhemoglobin (HHbO2). One molecule of Нb
attaches 4 molecules of oxygen. 1 g of Нb binds 1,34 ml of О2.
 Transport of СО2.
 Participates in maintenance of acid-alkaline state (hemoglobin buffer).
Bonds of Нb:
1. Оxyhemoglobin (НHbО2). Hemoglobin is connected with О2. Arterial
blood contains about 98% of HHbO2, and venous — about 60%. After feedback of
О2 from НHb it is called the restored or reduced hemoglobin. Hemoglobin has high
affinity to oxygen.
2. Carbohemoglobin (НHbСО2) — bond of hemoglobin with СО2.
3. Мethhemoglobin (MetHb). It is formed under the influence of strong
oxidants (permanganate of a potassium, aniline, nitrites, a pyrogallol, etc.). Thus,
Fe2+ turns into Fe3+). This bond is firm and can not be disconnected.
4. Carboxyhemoglobin (НHbCО) — bond of hemoglobin with carbonic
oxide (CO). This bond is in 150–200 times stronger than that of НHbО2. At CO
0,1% concentration in air, 80% of Нb turns into carboxyhemoglobin. At
concentration of 1% of CO death occurs in a few minutes.
Physiological bonds of Hb are НHbО2 and НHbСО2.
Myoglobin — the respiratory pigment, or muscular hemoglobin contained
in skeletal muscles and myocardium. It has the big affinity to oxygen in com19
parison with hemoglobin. It binds up to 14% of О2 in organism. Its role consists in
muscle supply with oxygen at muscles contraction when capillars are pressed and
tissues do not receive blood. In this moment the main source of oxygen is
myoglobin which in the phase of muscles relaxation is filled with oxygen.
Synthesis of Нb takes place in erythroblasts in bone marrow.
The state of reduced amount of Hb in one unit of blood volume (more often
at decrease of the number of erythrocytes) is called anemia.
In males anemia is observed when Hb amount is less than 130 grams per
liter, in females — less than 120 grams per liter (at pregnancy — less than 110
grams per liter).
Types of Hb:
 HbP — (primitive) – is formed at 7–12 week of intra-uterine
development.
 HbF — fetus — at 9-th week of intra-uterine development.
 HbA — hemoglobin of adults-appears before birth.
НbF — has the big affinity with О2 and binds 60% of O2 at such partial
pressure of O2 (рО2) whereas HbA only 30%. Due to the given property, HbF
supplies tissue with oxygen low рО2 in arterial blood. Within the first year of life
HbF almost completely is replaced by HbA.
In norm, Hb concentration in blood of male varies within 130–160 grams per
liter, in female blood — 115–145 grams per liter.
3. Hemolysis and its varieties
Hemolysis — destruction of erythrocytes membrane accompanying with the
release of Hb into plasma (laky blood, or pellucid blood).
Kinds of hemolysis:
1. Mechanical (in vivo at impacts on the body, in vitro at stirring blood in
the vial).
2. Thermal (in vivo at burns, in vitro at freezing and de-freezing of blood)
3. Chemical (in vivo under influence of chemical materials, at aspiration of
volatiles (acetone, benzene, chloroform), destruction of erythrocytes membrane in
vitro under influence of acids, alkalis, heavy metals, etc.).
4. Electrical (in vivo at affection by electric current, in vitro at transit of
electric current through blood in the vial). On the anode (+) is hemolysis acid, on
the cathode (-) — alkaline.
5. Biological. Under influence of factors of biological nature (hemolysins,
poison of snakes, fungal poison).
 6. Osmotic. In hypotonic solutions in person hemolysis begins in 0,48% of
NaCl solution, and in 0,32% — full hemolysis of erythrocytes.
Osmotic resistance of erythrocytes (ОRE) — their stability in hypotonic
solutions.
Distinguish:
Minimal ОRE — concentration of NaCl solution at which the hemolysis
(0,48–0,46%) begins.
Maximal ОRE — concentration of NaCl solution, at which all erythrocytes
are destructed (0,34–0,32%).
The osmotic resistance of erythrocytes depends on degree of their maturity
and form.
The young forms of erythrocytes are formed of the bone marrow of blood
and are more resistant to hypotonia.
7. Immune hemolysis — at transfusion of incompatible blood or at presence
of immune antibodys to erythrocytes.
8. Physiological — hemolysis of old erythrocytes in the end of their life (in
liver, spleen, a red bone marrow).

4. Erythrocyte sedimentation rate

If to prevent blood from coagulation (with the help of an anticoagulant) and
to let it stand, sedimentation of erythrocytes is observed.
Erythrocyte sedimentation rate (ESR) in norm is:
in men 1–10 mm / hour;
in women 2–15 mm / hour;
in newborn 1–2 mm / hour.
ESR depends on:
Properties of plasma:
 ESR is accelerated due to increase of concentration of molecules of
large globulins and fibrinogen in particular. Their concentration raise
at inflammatory processes, pregnancy. They reduce the electrical
charge of erythrocytes, promoting cohesion of erythrocytes and
formation of monetary columns.
 ESR decreases at augmentation of amount of erythrocytes (for
example, sedimentation of erythrocytes can stop completely owing to
increase of blood viscosity). At anemias ESR it is accelerated.
 ESR goes down at change of the form of erythrocytes (drepancytic
anemia).
 ESR it is slowed down at the decrease of рН and, vice versa,
accelerated at the increase of рН.
 The erythrocytes sedimentation rate increases at the increase of
hemoglobin concentration in cells.
 5. Leucocytes, their classification, features and functions

Leucocytes, or white blood cells, opposite to erythrocytes, have nucleus and

other structural elements peculiar to cells. The dimension from 7,5 up to 20
micrometres.
Functions of leucocytes:
 Protective (participation in maintenance of nonspecific and cell
immunodeficiency).
 Metabolic (release into digestive system, seizure of nutrients and their
transmission to blood. Especially, it has essential value in
maintenance of immunity in a newborn in the period of breast feeding.
 Dissolution of damaged tissues;
 Morphogenetic — destruction of various malformations in embryonic
period.
Functions of separate kinds of leucocytes:
1. agranular:
а) мonocytes — 2–10% of all leucocytes (macrophags). They are the largest
blood cells, have bactericidal activity, appear in affection spot after neutrophils. In
tisues monocytes turn into tissue macrophags.
In the affection spot they perform phagocytosis of:
 Microorganisms.
 died leucocytes.
 Damaged cells of a tissue.
They thus clear the affection area.
b) Lymphocytes — 20–40% from all leucocytes.
Opposite to other forms of leucocytes, after release from vessels they do not
come back and their life period is from some days, as in other leucocytes, to 20 and
more years.
Lymphocytes are the central part of immune system of an organism. They
provide with genetic constant of an organism.
They carry out:
 Antibody formation.
 Destruction of alien cells.
 Provide reaction of a transplant rejection.
 Keep immune memory.
 Destruction of own mutant cells.
 State of sensibilization.
Distinguish between:
T-lymphocytes (provide cellular immunodeficiency):
а) Т-assistants.
b) Т-suppressors.
c) Т-killers.
 d) Т-accelerators.
f) immune memory.
Bursacytes (provide non-cellular immunity).
Lymphocytes are formed from the common founder cell. The differentiation
of T-lymphocytes occurs in thymus gland, and bursacytes — in red bone marrow,
tonsils, lymph nodes, appendix.
Zero lymphocytes. They make 10–20% of all lymphoid cells.
2. Granular:
а) neutrocytes — the biggest groups of leucocytes (50–70% of all
leucocytes). They possess high bactericidal activity. They are carriers of receptors
to IgG, to proteins of complement. They first appear in the affection area destroy
harmful agents. One neutrophil is capable to destroy 20–30 bacteria.
b) Eosinocytes — 1–5% of all leucocytes (stained with eosin). It stays in
blood for some hours then migrate into tissues where they are destructed.
Functions of eosinocytes:
1. Phagocytosis.
2. Neutralization of toxins of the albuminous nature.
3. Destruction of alien proteins and antigen-antibody complexes.
4. Production of plasminogen, i.e. participation in fibrinolysis.
Their amount increases at helminthosis. They perform effect in struggle
against helminthes, their eggs.
c) Basophils — 0–1% of all leucocytes.
They produce histamin and heparin (they are called heparinocytes). Heparin
prevents coagulation of blood, histamin dilates capillars, promotes resorption and
healing of wounds.
Amount of leucocytes in norm: 4–9 × 109 per litre.
The increase of amount of leucocytes is called leucocytosis. There are the
following kinds of leucocytosis:
Physiological. It is caused by redistribution of leucocytes between vessels
and organs.
Physiological kinds of leucocytosis are:
1. Nutrition. After reception of nutrition as the result of release of leucocytes
into blood circulation from depot. Their accumulation in sub-mucous layer of
intestine where they carry out protective function.
2. Muscular. Under influence of heavy muscular work the quantity of
leucocytes grows in 3–5 times.
3. Pregnant. Leucocytes are accumulated in sub-mucose of a uterus.
4. Newborn (metabolic function).
. At pains.
6. At emotions.
Pathological — connected to diseases, infection contaminations, purulent,
inflammatory, septic and allergic processes.
 Leucocythemia — uncontrollable formation of leucocytes. Leucocytes in
these cases are poorly differentiated and do not carry out the physiological
functions.
Leucocytopenia (the amount of leucocytes is lower than 4×109 per litre).
Lifetime of various forms of leucocytes differs (from 2–3 days till 2–3 weeks).
Long-living lymphocytes (cells of immune memory) live for decades.

6. Thrombocytes, their structure, behavior and functions

Thrombocytes or blood a plate — the irregular round form the with length of
1–4 microns, and depth 0,5–0,75 microns.
Their amount in blood — 180–320×109 /l. They are formed in red bone
marrow by separation from the part of protoplasm of megakariocyte. One
megalokariocyte forms 3–4 thousand thrombocytes. 2/3 thrombocytes circulate in
blood, others are situated in spleen.
Constitution.
Range of cytoplasm directly adjoining to an environment is not structured.
The central part of cytoplasm contains granules.
Distinguish beads of 3 type:
α granules — contain blood-coagulation factors.
ß granules — the enzymes participating in a metabolism in a thrombocyte.
γ granules — tubules with englobed particles.
Thrombocytes are capable to englobe abiological foreign bodys, viruses,
cell-bound immune complexes, i.e. participate in nonspecific protective system of
an organism.
Duration of their life in blood is 5–11 days, then they are destroyed in liver,
lungs and spleen.
Upon destruction of thrombocytes the following materials are released:
Participate in blood coagulation.
Promote angiospasm — serotonin (F10), adrenalin, noradrenalin.
Produce adhesion and aggregation of thrombocytes.
There are daily fluctuations of thrombocytes number: in the afternoon the
amount of them increases, at night – it goes down. One of the basic functions of
thrombocytes is their participation in coagulation of blood.
 Lecture 3

Theme: Hemostasis

Plan:
1. Blood coagulation system.
2. Vascular platelet hemostasis.
3. Coagulating hemostasis.
4. Blood anticoagulating system.
5. Fibrinolysis.
6. Blood aggregate state regulation.

1. Blood coagulation system

Maintenance of blood in a fluid state and its ability to circulate in blood

vessels is a necessary condition for keeping up of an organism. It is ensured by the
regulation system of liquid state of blood.
This system includes:
• Coagulations system of blood (microvascular and coagulation hemostasis);
• Anticoagulating system of blood (anticoagulants and fibrinolysis).
• Mechanisms of regulation. Disturbance of blood coagulation is the basis of
many human diseases. Hemostasis (termination of bleeding) - is caused by:
• Spasm of blood vessels;
• Coagulations of blood and formation of thrombus.
System of hemocoagulation:
•Blood and tissues which produce and secrete materials participating in the
given process.
•Neuro-humoral regulating mechanism.

2. Vascular platelet hemostasis. (initial)

In a healthy person the termination of a bleeding in microcirculatory flow

with low arterial pressure is caused by realization of processes including:
1. Reflex spasm of damaged vessels (caused by release of noradrenalin,
adrenalin, serotonin at irritation of receptors). It is known as initial angiospasm.
2. Adhesion (attaching) of thrombocytes to damaged surfaces (the injured
area becomes positively (+) charged and thrombocytes have negative electrical
charge (-)). With participation of receptors they are attached to collagen in the
damaged area of the vessel.
3. Accumulation and aggregation of thrombocytes at the damaged focus.
Stimulators of the given process are adrenalin, thrombin, Са++, thromboplastin,
released from thrombocytes and erythrocytes (internal system), and collagen
released from cells of tissues of the damaged vessel (external system). In result, the
platelet thromb is formed. Aggregation of thrombocytes in this stage has reversible
character.
4. Irreversible aggregation of thrombocytes. Thrombocytes flow into
uniform mass, forming a thromb not penetrable for blood plasma. Reaction is
influenced by thrombin which is released from destroyed thrombocytes which
results in release of physiologically active substances: adrenalin, noradrenalin,
serotonin, nucleotides, blood-coagulation factors. They promote secondary spasm
of a vessel. Excreted in such way F3-platelet thromboplastin (thrombo-plastic
factor) starts the mechanism coagulating hemostasis. The small amount of fibrin is
formed.
5. Compression of platelet thrombus. Compression of thrombus is ensured
by protein of thrombocytes - thrombostenin (F6) and fibrin. It results in
termination of bleeding.
In fine vessels the hemostasis stops at this stage. Such kind of the hemostasis
refers to as initial, or microvascular.
In large vessels, with high blood pressure, platelet thrombus is not held up
and washed away. In similar vessels on the basis of such mechanism stronger
thrombus is formed as result of another mechanism — coagulating, or secondary
hemostasis.

3. Coagulating hemostasis

Coagulating hemostasis includes the following:

• Plasma blood-coagulation factors.
• Blood-coagulation factors of uniform elements of blood.
• Tissue blood-coagulation factors.
I. Plasma factors (marked chronologically in Roman figures).
• FI — fibrinogen. Protein of plasma. Concentration in blood is 3 g/l,
formed in liver. It is also a building stuff at healing wounds.
• FII — thrombinogen. Synthesized in liver with the presence of vitamin K.
•FIII — thromboplastin.
• FIV — calcium ions (Ca++). About 1/2 of Сa ++ are not connected with
the protein and 1/2 are in the complex with proteins of plasma. FIV is necessary in
all phases of blood coagulation. It promotes aggregation of thrombocytes, binds
heparin. 25
• FV — proaccelerin. It is formed in liver. Participates in the 1st and 2nd
phases of blood coagulation.
• FVI — it is excluded from classification.
• FVII — proconvertin. This is glycoprotein which is formed in liver with
the presence of vitamin K. It is necessary for formation of tissue thromboplastin.
 • FVIII — аntigemophilic globulin A. Formed in liver, spleen and
leucocytes. It activates prothrombin. It ensures optimum conditions for interaction
of factors IX and X. It is necessary for adhesion of thrombocytes and activation of
prothromboplastin. At absence of this factor hemophilia A occurs.
• FIX — аntigemophilia globulin B. Glycoprotein. At absence of this factor
hemophilia B occurs.
• FX — factor Stuart -Pruyr. Is part some tissue and blood thromboplastin. •
FXI — plasma predecessor of thromboplastin. It is necessary for activation of
blood thromboplastin, activates FIX. At absence of this factor hemophilia C
occurs.
• FXII — factor Hagemun - is activated at contact with an alien surface (for
example, a place of the damaged vessel) that is why him name the contact factor. It
is the initiator of formation of blood prothromboplastin and all process
hemocoagulation. At absence of this factor hemophilia D occurs.
• FXIII — fibrinstabilization factor. Contains in plasma, cells and in tissue.
It is necessary for formation of final or unsolvable fibrin. It is activated by
thrombin and Ca++. At deficiency of the given factor badly heal wounds.
Phases of coagulating hemostasis:
• 1st phase — formation active thromboplastin (tissue and blood). Process
goes with participation of tissue and plasma factors: IV, V, VIII, IX, X, XI.
Formation of thromboplastin takes place as a result of interaction of lipid factor
with plasma factors. Blood thromboplastin is formed from destroyed blood cells
(internal system). Tissue thromboplastin is released from damaged cells of walls of
vessels and tissues. Thromboplastin is necessary for thrombinogen activation.
• II phase — activation of inactive thrombinogen into active form —
thrombin. This process is influenced by FVI — pro-accelerin (accelerin), FVII —
convertin, Ca++ and some factors of thrombocytes.
• III phase — transformation process of soluble fibrinogen into unsoluable
form — fibrin. Thrombin is necessary for proteolysis of fibrinogen molecule,
transforming of it into fibrin. Fibrinogen is formed in liver. Vitamin K is necessary
for its synthesis.
Under influence of thrombin with the presence of Ca++ the process of
insoluble fibrin formation goes in 3 stages:
• 1. Influenced by thrombin, fibrinogen is splitted into fibrin-monomers.
• 2. In result of polymerization of fibrin-monomers, the molecule of soluble
fibrin — polymer «S» is formed. For polymerization presence of Calcium ions is
necessary.
• 3. Under influence of fibrinstabilization factor (FXIII) the insoluble fibrin
("I") is formed.
Uniform elements of blood get stuck into fibrin nets, thus forming the blood
thrombus. Such thrombus is subject to compression influenced by protein
trombostenin. At compression of thrombus the periphery of the wound are closing.
Time of blood coagulation is 5–7 min.

4. Blood anticoagulating system

Despite the fact that all factors necessary for blood coagulation constantly
circulate in blood, it remains fluid. It is one of parameters of homeostasis.
Mechanisms of maintaining of blood liquidity:
• Smooth surface of vessels (prevents activation of Hagemun factor and
aggregation of thrombocytes).
• Negative charges of wall of vessels and uniform elements of blood that
provides their repulsion from each other.
• Wall of vessels is coated with thin layer the soluble fibrin having ability to
adsorb active blood-coagulation factors.
• High blood flow rate (interferes concentration of coagulation factors)
• Presence of natural anticoagulants.
In the organism there are 2 groups of anticoagulants:
• 1. Initial (constantle presenting in blood).
• 2. Secondary (formed during coagulation or fibrinolysis).
Initial anticoagulants — antithromboplastins, antithrombins:
• Antithrombin II (heparin). It inhibits all phases of hemocoagulation.
• Antithrombin III — plasma factor of heparin. It transforms thrombin into
inactive metathrombin.
• Antithrombin IV.
• Protein C — vitamin К-dependent protein. Activates fibrinolysis.
• Тromboxane — Inhibits aggregation of thrombocytes. Secondary
anticoagulants.
The function of secondary anticoagulants consists in restriction of
intravascular coagulation.
• Antithrombin I (fibrin) is capable to absorb significant (up to 90%) amount
of thrombin.
• Anticoagulants formed at fibrinolisis (products of degradation of
thrombinogen, fibrinogen and fibrin).
Anticoagulants used in laboratory clinical practice:
• 1. Heparin.
• 2. Citric acid and its 0,5% salt solutions.
Factors accelerating blood coagulation:
• Affection of wall of vessels.
• Augmentation of thromboplastin formation.
• Augmentation of vitamin K absorption in an organism.
• Augmentation of fibrinogen formation.
• Temperature increase.
 • Increased contents of amino acids in blood.
• Decrease of fibrinolysis process. Factors decreasing coagulation
• Decrease of thromboplastin formation.
• Decrease of vitamin K absorption.
• Increased development of anticoagulants.
• Decrease of fibrinogen formation.
• Type A hemophilia — terminated phase I of coagulation (disturbance of
thromboplastin formation). At absence of FVIII, phases II and III are also
terminated.
• Type B hemophilia — absence of FIX.
• Type C hemophilia — absence of FXI (plasma precursor of
thromboplastin).
• Type D hemophilia — absence of FXII. In men hemophilia is met more
often than in women.

5. Fibrinolysis

Fibrinolysis — dilution of blood thrombus. It is considered that in blood

there is constant transformation of small amount of fibrinogen into fibrin which is
exposed to dilution — fibrinolysis.
Only at damage of tissue the process of formation of fibrin dominates
fibrinolysis and local blood coagulation takes place. The main function of
fibrinolysis — regeneration of lumen of a blood vessel.
Fibrinolysis starts immediately upon thrombus compression in 2 phases:
I phase plasminogen transformation into plasmin.
II phase — plasmin-influenced dilution of fibrin (thrombus) with formation
of peptides and amino acids.
Factor providing fibrinolysis is the plasminogen which under influence of
tissue and blood factors transform into the active form - plasmin.

6. Blood aggregate state regulation

In the norm there is no intravascular coagulation of blood or it occurs in very

insignificant degree. The fragile regulation process of blood coagulation involves
many factors and systems:
• Presence of the number of inhibitors pro-coagulants in plasma.
• Many factors are in inactive state.
• Concentration of pro-coagulants decreases due to fibrinolysis. Therefore,
thrombus is not formed in vessels with the fast blood flow but appears in vessels
with low blood flow.
• Pro-coagulants inactivate in blood.
 On the whole, the mechanism of coagulation regulation is neuro-humoral. In
the organism there are special chemoreceptors reacting to thrombin, plasmin and
other factors coagulation and anticoagulation systems concentration in blood.
Stimulation of sympathetic nervous system increases the speed of blood
coagulation (hypercoagulation). It is marked at stressful states, pains,
accompanying with release of adrenalin.
Under the influence of adrenalin:
• Thromboplastin is released from the vascular wall.
• FXII (the contact factor) is induced which activates prothromboplastin.
• Phospholipids are released from erythrocytes.
• Glycocorticoids, somatotropic hormone, antidiuretic hormone, Calcitonin,
testosteron, progesteron primarily cause hypercoagulation but once again activate
fibrinolysis.
Blood coagulation is prevented by action complex anticoagulation
mechanism.
• At appearance in vessels of slowly formed thrombin it is neutralized by
plasma anticoagulants antithrombins, heparin).
• Heparin:
• Prevents formation of thromboplastin and thrombin, alongside activating
fibrinolysis.
Stimulation of parasympathetic nervous system (n. vagus) results in the
same effects as stimulation of sympathetic nerves.

Lecture 4

Theme: Blood groups. Blood system regulation

Plan: 1. Blood groups. Fundamentals of blood transfusion.

2. Rhesus-factor.
3. Blood system regulation.
4. Blood substituting solution.

1. Blood groups.

Fundamentals of blood transfusion In 1901 Charles Landshtener observed

that at blending of blood from different people in one case there was an
agglutination of erythrocytes, in other cases it was absent. His further research and
also that of J. Jansky allowed to establish blood groups which differ from each
either by presence or absence of erythrocytes of antigens (agglutinogens) and
antibodies (agglutinins) in plasma (tabl. 3).

Table 3
 Blood groups of system AB0

Blood groups Erythrocytes Plasma or serum

Аgglutinogen Аgglutinin
I (0) 0 α, ß
II (A) A ß
III (B) B α
IV (AB) AB 0

Аgglutinogens of erythrocytes (A and В). With them, γ-globulin-natured

specific antibodies (agglutinins α and ß) dissolved in the plasma incorporate. They
have 2 centers of linkage that provides an opportunity of formation of the bridges
between two erythrocytes and thus formation of erythrocytes conglomerates.
In norm in each person agglutinins to corresponding agglutinogens are
absent, i.e. each person has individual panel of erythrocytes of agglutinogens.
In blood of a neonatal there are no antibodies of system AB0 and their
formation to antigens absent in the newborn, happens within the first year of life.
At blood transfusion they select blood to avoid meeting of similar
аgglutinogens of the donor with agglutinins of the recipient (e.g. A and α, B and
ß). Agglutinins of the donor are not considered since there is their dilution in the
blood of the recipient and they cannot cause agglutination of his erythrocytes (at
transfusion of small amounts of blood of 200–500 ml). At transfusion of big
amount (4–5 l) of blood plasma of 0 (I), a big number of agglutinins comes into the
recipient’s blood. Thus dilution effect is lost and therefore agglutinins of the donor
may cause agglutination of erythrocytes of the recipient.
As a rule, they transfuse only identical blood (e.g. 1st group blood with the
1st group blood). With its absence in emergency cases blood transfusion is
performed under scheme of blood groups compatibility (tabl. 4).
Table 4

Compatibility of various blood groups

Serum group Erythrocyte group
I (0) II (A) III (B) IV (AB)
I α, ß – + + +
II ß – – + +
III α – + – +
IV – – – –

Note: «+» — presence of agglutination (group incompatibility); «–» —

absence of agglutination (group compatibility).
 Persons with the I (0) blood group are known as universal donors, those with
the IV (АВ) group — universal recipients.
To avoid complications at blood transfusion:
1. They determine blood group with application of standard serum of I, II
and III groups by blending of a drop from each serum kind with the drop of the
examined blood. By presence or absence of agglutination in them group
compatibility is determined. To avoid mistakes, examination is conducted at
temperature of 15–25°C. The drop of blood brought into serum should be in 3–5
times less than serum drop volume. In case of indistinct results, examination is
repeated with serum of other series. Should the doubtful result is obtained again,
direct and reverse test is carried out:
Direct test. The donor’s erythrocytes are mixed on a slide with plasma or
serum of a recipient at 37°С. Its purpose is to determine presence of antibodies in
serum of the recipient to erythrocytes of the donor. If there is no agglutination,
reverse test is carried out. Erythrocytes of recipient are placed into serum of the
donor in order to reveal antibodies in serum of the donor to erythrocytes of the
recipient.
2. Biological test is carried out. First, they perform stream intravenous
introduction of 10–15 ml of donor blood and for 3–5 min the patient is watched for
presence or absence of complications (heart and respiration rate increase, short-
breath, heavy breathing, face hyperemia, etc.). Such introduction is repeated for
three times. At absence of any complications the rest portion of blood is
administered.
In people with I (0) blood group аnti-A and аnti-B immune agglutinins, i.e. ά
and ß, present in plasma. Transfusion of such blood in big amounts is prohibited
since in these cases agglutinins of the donor are not dissolved in plasma of the
recipient and can cause agglutination of erythrocytes of the recipient. Besides, in
persons with I (0) blood group antigen Н presents on surface of erythrocytes
which can interact with аnti-H-antibodes frequently met in blood plasma of II (A)
and IV (АВ) groups and little bit less in III (В)group. In these cases blood
transfusion of I (0) group to the persons having other blood groups can result in
hemotransfution shock. Therefore universal donors are called dangerous universal
donors.
Presence of the Н-antigen on a surface of erythrocytes ensured name of AB0
system as АВН.
Prevalence of people with blood groups: I (0) — 40–50%, II (А) — 30–
40%, III (В) — 10–20%, IV (АВ) — 5%. Geography: 40% of people of Central
Europe have blood group II (А), 90% of North America — I (0), more than 20% of
Central Asia — III (В). I (0) blood group presents in all nationalities, II (А) —
dominates at inhabitants of Europe, Mid East, China, Japan. People with III (В)
blood group are the least, IV (АВ) dominates in inhabitants of India, Central Asia,
valley of Nile.
 Apart from agglutinogens A and B (systems AB0), more than 400
agglutinogens are known, 140 from which (M, N, S, P, Di, C, K, Ln, Le, Fy, Ik,
etc.) make almost 20 groups or systems.
From them, it is possible to note systems: MNSS, P, Lutherans, Lewis, Kidd,
etc. For example, system Kell-Chellano consists of 2 agglutinogen K and k and
forms 3 groups — KK, кк and Кк. The given system of blood presents in 100% of
people.
Fortunately, antigenic properties of the majority of these antigens are poorly
expressed and neglected at blood transfusion. However, these systems matter at
frequent blood transfusions. Therefore it is not recommended to repeat blood
transfusion from the same donor.
Alongside with аgglutinins, blood plasma contains hemolysins (marked
agglutinins α and ß respectively). When met with similar agglutinogens they result
in hemolysis of erythrocytes. Their action is revealed at temperature of 37–40°C
and in 30–40 seconds hemolysis of erythrocytes happens.

2. Rhesus-factor

The Rh-factor (Rh) was discovered in 1940 by Landschtaner and Wiener. It

presents in 85% of people blood has this factor, in 15% it is absent. People whose
blood has Rh-factor are called rhesus — positive (Rh+ ), those who have not are
rhesus - negative (Rh- ).
The Rh-factor includes 6 basic antigens: C, D, E, c, d, e. From them, the
most powerful is D (it possesses the increased antigenic properties).
At transfusion of Rh+ blood to the Rh- person the аgglutinins formation in
such recipient lasts slowly (within several months). That’s why at single
transfusion hemotransfutions complications are not observed. At the repeated
transfusion, rhesus-incompatibility (rhesus-conflict) with serious hemotransfutions
complications occurs: formation of conglomerates of erythrocytes and their
hemolysis, intensive intravascular blood coagulation, many organs are affected,
kidneys in particular.
It is important to take into account rhesus-factor of a mother at pregnancy. If
the fetus inherits Rh-positive blood from the father, and the mother is Rhnegative,
in this case antibodies to Rh+ erythrocytes of fetus are formed in the mother’s
organism. Formation of Rh in fetus starts only from the 3rd month of antenatal
period and becomes active by the end of pregnancy. During this period the
organism of the mother has not time for sensibilization. Formation an antirhesus —
аgglutinins lasts slowly (3–5 months). Therefore, at the first pregnancy
complications are almost not observed. At repeated pregnancy there is a rhesus —
conflict menace at which erythrocytes of fetus are destroyed which can result in his
intra-uterine death.
 For depressing of antibody formation to Rh, аnti-D-prevention is performed
in the mother’s organism, i.e. they administer immune serum to the mother
instantly upon delivery. This serum contains аnti-D-globulin which destroy Rh+
erythrocytes of the fetus which got into blood of mother, i.e. the factor causing
antibody formation and their accumulation is destroyed.

3. Blood system regulation

Erythrogenesis.
Neuro-humoral regulation erythrogenesis. For the normal erythrogenesis
process the normal nutrition sufficient amount of ferrous lactate is necessary. It is a
limitation factor. The lack of it results in anemia.
Erythropoietins are formed in many organs (lien, liver, bone marrow,
salivary glands) but most of all in kidneys. The basic starting mechanism is
hypoxia, or loss of blood.
Каstle’s аntianemic factor — complex of vitamin В12 (external factor) and
gastromycoproteid in belly (internal factor). This complex comes into liver and
from it into the bone marrow.
Ascorbic acid — promotes absorption of ferrous lactose into intestine
transmitting it from Fe+++ into Fe++. The daily need in ferrous lactose for
realization of normal erythrogenesis is 20–25 mg.
Products of erythrocytes destruction stimulate hemopoiesis
(autoregulation). The amount of the destroyed erythrocytes is equal to that of
newly formed erythrocytes (self-control).
Hormones. Аndrogens increase and estrogens decrease erythrogenesis. That
is why the number of erythrocytes in men’s blood is higher than in women.
Erythropiesis is stimulated by adrenalin, thyroxin, somatotropic hormone.
The role of nervous system. The irritation of the nerves going to the bone
marrow, enforces erythropiesis. Action of nervous and hormonal factors on red
bone marrow is carried out through erythropoitetins.
The role of cerebral cortex. It is possible to work out conditioned reflex
resulting in the decreased formation of erythrocytes.
Leukopoiesis.
Neuro-humoral regulation of leukopoiesis.
1. A stimulation of leukopoiesis by products of leukocytes destruction
(selfcontrol). The more destruction is, the higher is their formation.
2. Stimulation by tissue destruction products, especially by their proteins.
3. Stimulation by microbes and their toxins.
4. Stimulation of leukopoiesis by leukopoietins.
5. Hormones. Adrenalin, hydrocortisone result in leukocytosis due to release
from blood depot of neutrophils, моnocytes and lymphocytes (leukocytosis at
stress, emotional excitation).
 The role of nervous system. The irritation of sympathetic nervous system
increases the amount of neutrophils. The irritation of vagus reduces the amount of
leukocytes in blood of peripheric vessels.
Thrombocytopoiesis.
Thrombocytopoietins are of short and long action. The first are formed in
lien and stimulate release of thrombocytes into blood. The second are contained
contain in blood plasma and stimulate formation of thrombocytes in the bone
marrow.
Thrombocytopoiesis increases after loss of blood. In some hours the number
of thrombocytes can increase and exceed their normal amount in twice.

4. Blood substituting solution

At hemodynamic disorders caused by loss of blood, apart from blood

transfusion various blood substituting solutions are used. The latter should
conform with the following demands:
 By physico-chemical properties they should be close to the basic
parameters of blood (isotonic, isoionic, etc.).
 Absence of influence on basic biological properties of blood.
 Absence of toxicity.
 Long-term stay in vascular system.
 To maintain sterilization and long storage.
 Should not produce sensibilization of an organism and lead to
anaphylaxis shock at repeated introduction.
Salt solutions:
 Saline solution — 0,85–0,9% NaCl.
 Ringer-Lock’s solution.
 and other.
Since these solutions do not contain colloids they are quickly released from
blood channel, i.e. they can fill the amount of the lost blood within short period of
time.
Synthetic colloid blood substituting solutions (plasma substitutes).
Negative properties of colloid blood supplements are their ability to produce
allergic responses.
Protein preparations: native, preserved and fresh frozen plasma (FFP).
Solution albumin 5%.
Protein is an albuminous preparation of isogenic human plasma.
At their intravenous introduction the volume of circulating blood increases.
They bind toxic materials.
Transfusion of whole blood at present is applied rather seldom, they use for
transfusion only those components of blood which the organism needs much:
plasma, erythrocytes mass, etc.
 Preparations of blood: preserved blood, plasma, erytrocytes mass, washed
erythrocytes, leukocytes (fresh), thrombocytes (fresh).