Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Afk Seminar 2

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 14

ABSTRACT.

Respiratory control is accomplished by a complex, integrative control system with a difficult task to
assure homeostasis of blood oxygen and carbon dioxide throughout life. Multiple neural mechanisms
enable the respiratory control system to respond appropriately to changing environmental and
physiological conditions, including feedback and feed-forward mechanisms that are modified by
neuroplasticity. Ventilatory control disorders challenge homeostasis of respiratory gases, leading to
severe morbidity and mortality. By greater understanding of mechanisms regulating blood gas
homeostasis and pathological mechanisms of disease, new therapeutic approaches may be possible
to treat devastating ventilatory control disorders with no known cures.

Respiratory control is accomplished by a complex, integrative control system with a difficult task to
assure homeostasis of blood oxygen and carbon dioxide throughout life. Multiple neural mechanisms
enable the respiratory control system to respond appropriately to changing environmental and
physiological conditions, including feedback and feed-forward mechanisms that are modified by
neuroplasticity. Ventilatory control disorders challenge homeostasis of respiratory gases, leading to
severe morbidity and mortality. By greater understanding of mechanisms regulating blood gas
homeostasis and pathological mechanisms of disease, new therapeutic approaches may be possible
to treat devastating ventilatory control disorders with no known cures.
Respiratory control is accomplished by a complex, integrative control system with a difficult task to
assure homeostasis of blood oxygen and carbon dioxide throughout life. Multiple neural mechanisms
enable the respiratory control system to respond appropriately to changing environmental and
physiological conditions, including feedback and feed-forward mechanisms that are modified by
neuroplasticity. Ventilatory control disorders challenge homeostasis of respiratory gases, leading to
severe morbidity and mortality. By greater understanding of mechanisms regulating blood gas
homeostasis and pathological mechanisms of disease, new therapeutic approaches may be possible
to treat devastating ventilatory control disorders with no known cures.

DEFINITION
The neural control of respiration refers to functional interactions between networks of neurons
that regulate movements of the lungs, airways and chest wall and abdomen, in order to
accomplish
(i) effective organismal uptake of oxygen and expulsion of carbon dioxide, airway
liquids and irritants,
(ii) Regulation of blood pH.
INTRODUCTION
Respiration is crucial for animal survival. In the last 10 years, the cytoarchitecture
of the respiratory control center has been analyzed at the single-cell and genetic
levels. The respiratory center is located in the medulla oblongata and is involved
in the minute-to-minute control of breathing. Unlike the cardiac system,
respiratory rhythm is not produced by a homogeneous population of pacemaker
cells. Rather, it can be explained with two oscillators: the parafacial respiratory
group (pFRG;) and the pre-Bötzinger complex (preBötC,) The inspiratory and
expiratory activities produced in these medullary respiratory rhythm generators
are modulated from various sites of the lower brainstem, including the pons ) and
Bötzinger complex, and are then output as motoneuron activities through the
efferent networks in the brainstem and spinal cord (see Sects. 2 to 5). Different
types of preparations, mainly from mice and rats, have been used to analyze
respiratory rhythm and pattern generation, including: medullary slice preparation
in vitro (newborn or juvenile), en bloc brainstem-spinal cord preparation
(newborn), decerebrated and arterially perfused preparation in situ (newborn and
juvenile) and in vivo preparation (all ages). The normal respiratory motor pattern
basically consists of three or four phases: pre-inspiratory, inspiratory, postinspiratory, and
late-expiratory. However, the motor output patterns in the
different experimental models often display variation and the variations have
caused some controversies in the field. In the last decades, new knowledge has
been accumulated on the anatomical and physiological mechanisms underlying
respiratory rhythm generation and regulation.

CHAPTER 1

NERVOUS SYSTEM

DEFINITION

nervous system is organized group of cells specialized for the conduction of


electrochemical stimuli from sensory receptors through a network to the site

at which a response occurs. It is one of the integrating centers for homeostasis.


It is divided into:

1.Central Nervous system

2. Peripheral Nervous system.

CENTRAL NERVOUS SYSTEM


Central Nervous system (CNS) includes brain and spinal cord. It is formed by neurons and
supporting cells called neuroglia. Structures of brain and spinal cord are
Arranged in two layers,namely gray matter and white matter. Gray matter is formed by nerve ccel
bodies and The proximal parts of nerve fibers, arising from nerve cell body. White matter is
formed by remaining parts of nerve fibers.
In brain, white matter is placed in the inner part and Gray matter is placed in the outer part. In
spinal cord, whiite matter is in the outer part and gray matter is in the inner part. Brain is situated
in the skull. It is continued as spinal cord in the vertebral canal through the foramen magnum Of
the skull bone. Brain and spinal cord are surrounded By three layers of meninges called the outer
dura mater, middle arachnoid mater and inner pia mater. The space between arachnoid mater and
pia matter Is known as subarachnoid space. This space is filled with a fliud called cerebrospinal
fluid.

Brain and spinal cord are actually suspended in the cerebrospinal fluid.

PERIPHERAL NERVOUS SYSTEM

The peripheral nervous system (PNS) is one of two components that make up the nervous system
of bilateral animals, with the other part being the central nervous system (CNS). The PNS consists
of the nerves and ganglia outside the brain and spinal cord.[1] The main function of the PNS is to
connect the CNS to the limbs and organs, essentially serving as a relay between the brain and
spinal cord and the rest of the body.[2] Unlike the CNS, the PNS is not protected by the vertebral
column and skull, or by the blood–brain barrier, which leaves it exposed to toxins and mechanical
injuries.[3]

The peripheral nervous system is divided into the somatic nervous system and the autonomic
nervous system. In the somatic nervous system, the cranial nerves are part of the PNS with the
exception of the optic nerve (cranial nerve II), along with the retina. The second cranial nerve is not
a true peripheral nerve but a tract of the diencephalon.[4] Cranial nerve ganglia originated in the
CNS. However, the remaining ten cranial nerve axons extend beyond the brain and are therefore
considered part of the PNS.[5] The autonomic nervous system exerts involuntary
control over smooth muscle and glands.

citation needed] The connection between CNS and organs


allows the system to be in two different functional states: sympathetic and parasympathetic.
Chapter 2Boundless Anatomy and Physiology

Respiratory System

Respiration Control

Neural Mechanisms (Respiratory Center)

The medulla and the pons are involved in the regulation of the ventilatory pattern of
respiration.

Involuntary respiration is any form of respiratory control that is not under direct,
conscious control. Breathing is required to sustain life, so involuntary respiration allows
it to happen when voluntary respiration is not possible, such as during sleep. Involuntary
respiration also has metabolic functions that work even when a person is conscious.

The Respiratory Centers.

Involuntary respiration is controlled by the respiratory centers of the upper brainstem


(sometimes termed the lower brain, along with the cerebellum). This region of the brain
controls many involuntary and metabolic functions besides the respiratory system,
including certain aspects of cardiovascular function and involuntary muscle movements
(in the cerebellum).

The respiratory centers contain chemoreceptors that detect pH levels in the blood and
send signals to the respiratory centers of the brain to adjust the ventilation rate to
change acidity by increasing or decreasing the removal of carbon dioxide (since carbon
dioxide is linked to higher levels of hydrogen ions in blood).

There are also peripheral chemoreceptors in other blood vessels that perform this
function as well, which include the aortic and carotid bodies.
The Medulla

The medulla oblongata is the primary respiratory control center. Its main function is to
send signals to the muscles that control respiration to cause breathing to occur. There
are two regions in the medulla that control respiration:

 The ventral respiratory group stimulates expiratory movements.


 The dorsal respiratory group stimulates inspiratory movements.

The medulla also controls the reflexes for nonrespiratory air movements, such as
coughing and sneezing reflexes, as well as other reflexes, like swallowing and vomiting.

The Pons

The pons is the other respiratory center and is located underneath the medulla. Its main
function is to control the rate or speed of involuntary respiration. It has two main
functional regions that perform this role:

 The apneustic center sends signals for inspiration for long and deep breaths. It
controls the intensity of breathing and is inhibited by the stretch receptors of the
pulmonary muscles at maximum depth of inspiration, or by signals from the
pnuemotaxic center. It increases tidal volume.
 The pnuemotaxic center sends signals to inhibit inspiration that allows it to finely
control the respiratory rate. Its signals limit the activity of the phrenic nerve and
inhibits the signals of the apneustic center. It decreases tidal volume.

The apneustic and pnuemotaxic centers work against each other together to control the
respiratory rate.

Neural Mechanisms (Cortex)

The cerebral cortex of the brain controls voluntary respiration

Voluntary respiration is any type of respiration that is under conscious control. Voluntary
respiration is important for the higher functions that involve air supply, such as voice
control or blowing out candles. Similarly to how involuntary respiration’s lower functions
are controlled by the lower brain, voluntary respiration’s higher functions are controlled
by the upper brain, namely parts of the cerebral cortex.

The Motor Cortex

The primary motor cortex is the neural center for voluntary respiratory control. More
broadly, the motor cortex is responsible for initiating any voluntary muscular movement.
The processes that drive its functions aren’t fully understood, but it works by sending
signals to the spinal cord, which sends signals to the muscles it controls, such as the
diaphragm and the accessory muscles for respiration. This neural pathway is called the
ascending respiratory pathway.

Different parts of the cerebral cortex control different forms of voluntary respiration.
Initiation of the voluntary contraction and relaxation of the internal and external
intercostal muscles takes place in the superior portion of the primary motor cortex.

The center for diaphragm control is posterior to the location of thoracic control (within
the superior portion of the primary motor cortex). The inferior portion of the primary
motor cortex may be involved in controlled exhalation.

Activity has also been seen within the supplementary motor area and the premotor
cortex during voluntary respiration. This is most likely due to the focus and mental
preparation of the voluntary muscular movement that occurs when one decides to
initiate that muscle movement.

Note that voluntary respiratory nerve signals in the ascending respiratory pathway can
be overridden by chemoreceptor signals from involuntary respiration. Additionally, other
structures may override voluntary respiratory signals, such as the activity of limbic
center structures like the hypothalamus.

During periods of perceived danger or emotional stress, signals from the hypothalamus
take over the respiratory signals and increase the respiratory rate to facilitate the fight or
flight response.

Nerves Used in Respiration

There are several nerves responsible for the muscular functions involved in respiration.
There are three types of important respiratory nerves:

 The phrenic nerves: The nerves that stimulate the activity of the diaphragm. They
are composed of two nerves, the right and left phrenic nerve, which pass through
the right and left side of the heart respectively. They are autonomic nerves.
 The vagus nerve: Innervates the diaphragm as well as movements in the larynx
and pharynx. It also provides parasympathetic stimulation for the heart and the
digestive system. It is a major autonomic nerve.
 The posterior thoracic nerves: These nerves stimulate the intercostal muscles
located around the pleura. They are considered to be part of a larger group of
intercostal nerves that stimulate regions across the thorax and abdomen. They are
somatic nerves.
These three types of nerves continue the signal of the ascending respiratory pathway
from the spinal cord to stimulate the muscles that perform the movements needed for
respiration.

Damage to any of these three respiratory nerves can cause severe problems, such as
diaphragm paralysis if the phrenic nerves are damaged. Less severe damage can
cause irritation to the phrenic or vagus nerves, which can result in hiccups.

Chapter 3

Chemoreceptor Regulation of Breathing

Chemoreceptors detect the levels of carbon dioxide in the blood by monitoring the
concentrations of hydrogen ions in the blood

Chemoreceptor regulation of breathing is a form of negative feedback. The goal of this


system is to keep the pH of the blood stream within normal neutral ranges, around 7.35.

Chemoreceptors

A chemoreceptor, also known as chemosensor, is a sensory receptor that transduces a


chemical signal into an action potential. The action potential is sent along nerve
pathways to parts of the brain, which are the integrating centers for this type of
feedback. There are many types of chemoreceptors in the body, but only a few of them
are involved in respiration.

The respiratory chemoreceptors work by sensing the pH of their environment through


the concentration of hydrogen ions. Because most carbon dioxide is converted to
carbonic acid (and bicarbonate ) in the bloodstream, chemoreceptors are able to use
blood pH as a way to measure the carbon dioxide levels of the bloodstream.

The main chemoreceptors involved in respiratory feedback are:

1. Central chemoreceptors: These are located on the ventrolateral surface of medulla


oblongata and detect changes in the pH of spinal fluid. They can be desensitized
over time from chronic hypoxia (oxygen deficiency) and increased carbon dioxide.
2. Peripheral chemoreceptors: These include the aortic body, which detects changes
in blood oxygen and carbon dioxide, but not pH, and the carotid body which
detects all three. They do not desensitize, and have less of an impact on the
respiratory rate compared to the central chemoreceptors.

Chemoreceptor Negative Feedback

Negative feedback responses have three main components: the sensor, the integrating
sensor, and the effector. For the respiratory rate, the chemoreceptors are the sensors
for blood pH, the medulla and pons form the integrating center, and the respiratory
muscles are the effector.

Consider a case in which a person is hyperventilating from an anxiety attack. Their


increased ventilation rate will remove too much carbon dioxide from their body. Without
that carbon dioxide, there will be less carbonic acid in blood, so the concentration of
hydrogen ions decreases and the pH of the blood rises, causing alkalosis.

In response, the chemoreceptors detect this change, and send a signal to the medulla,
which signals the respiratory muscles to decrease the ventilation rate so carbon dioxide
levels and pH can return to normal levels.

There are several other examples in which chemoreceptor feedback applies. A person
with severe diarrhea loses a lot of bicarbonate in the intestinal tract, which decreases
bicarbonate levels in the plasma. As bicarbonate levels decrease while hydrogen ion
concentrations stays the same, blood pH will decrease (as bicarbonate is a buffer) and
become more acidic.

In cases of acidosis, feedback will increase ventilation to remove more carbon dioxide
to reduce the hydrogen ion concentration. Conversely, vomiting removes hydrogen ions
from the body (as the stomach contents are acidic), which will cause decreased
ventilation to correct alkalosis.

Chemoreceptor feedback also adjusts for oxygen levels to prevent hypoxia, though only
the peripheral chemoreceptors sense oxygen levels. In cases where oxygen intake is
too low, feedback increases ventilation to increase oxygen intake.

A more detailed example would be that if a person breathes through a long tube (such
as a snorkeling mask) and has increased amounts of dead space, feedback will
increase ventilation.

Proprioceptor Regulation of Breathing

The Hering–Breuer inflation reflex prevents overinflation of the lungs.

The lungs are a highly elastic organ capable of expanding to a much larger volume
during inflation. While the volume of the lungs is proportional to the pressure of the
pleural cavity as it expands and contracts during breathing, there is a risk of over-
inflation of the lungs if inspiration becomes too deep for too long. Physiological
mechanisms exist to prevent over-inflation of the lungs.
The Hering–Bauer Reflex

The Hering–Breuer reflex (also called the inflation reflex) is triggered to prevent over-
inflation of the lungs. There are many stretch receptors in the lungs, particularly within
the pleura and the smooth muscles of the bronchi and bronchioles, that activate when
the lungs have inflated to their ideal maximum point.

These stretch receptors are mechanoreceptors, which are a type of sensory receptor
that specifically detects mechanical pressure, distortion, and stretch, and are found in
many parts of the human body, especially the lungs, stomach, and skin. They do not
detect fine-touch information like most sensory receptors in the human body, but they
do create a feeling of tension or fullness when activated, especially in the lungs or
stomach.

When the lungs are inflated to their maximum volume during inspiration, the pulmonary
stretch receptors send an action potential signal to the medulla and pons in the brain
through the vagus nerve.

The pneumotaxic center of the pons sends signals to inhibit the apneustic center of the
pons, so it doesn’t activate the inspiratory area (the dorsal medulla), and the inspiratory
signals that are sent to the diaphragm and accessory muscles stop. This is called the
inflation reflex.

As inspiration stops, expiration begins and the lung begins to deflate. As the lungs
deflate the stretch receptors are deactivated (and compression receptors called
proprioreceptors may be activated) so the inhibitory signals stop and inhalation can
begin again—this is called the deflation reflex.

Early physiologists believed this reflex played a major role in establishing the rate and
depth of breathing in humans. While this may be true for most animals, it is not the case
for most adult humans at rest. However, the reflex may determine the breathing rate
and depth in newborns and in adult humans when tidal volume is more than 1 L, such
as when exercising.

Additionally, people with emphysema have an impaired Hering–Bauer reflex due to a


loss of pulmonary stretch receptors from the destruction of lung tissue, so their lungs
can over-inflate as well as collapse, which contributes to shortness of breath.

Sinus Arrhythmia

As the Hering–Bauer reflex uses the vagus nerve as its neural pathway, it also has a
few cardiovascular system effects because the vagus nerve also innervates the heart.
During stretch receptor activation, the inhibitory signal that travels through the vagus
nerve is also sent to the sinus-atrial node of the heart. Its stimulation causes a short-
term increase in resting heart rate, which is called tachycardia.

The heart rate returns to normal during expiration when the stretch receptors are
deactivated. When this process is cyclical it is called a sinus arrhythmia, which is a
generally normal physiological phenomenon in which there is short-term tachycardia
during inspiration.

Sinus arryhthmias do not occur in everyone, and are more common in youth. The
sensitivity of the sinus-atrial node to the inflation reflex is lost over time, so sinus
arryhthmias are less common in older people.

REFERENCE

Ballanyi K, Onimaru H, Homma I (1999) Respiratory network function in the


isolated brainstem-spinal cord of newborn rats. Prog Neurobiol 59:583–
634PubMedCrossRefGoogle Scholar

Bianchi AL, Denavit-Saubie M, Champagnat J (1995) Central control of


breathing in mammals: neuronal circuitry, membrane properties and
neurotransmitters. Physiol Rev 75:1–45PubMedGoogle Scholar

1. 3.

Bonham AC (1995) Neurotransmitters in the CNS control of breathing. Respir


Physiol 101:219–230PubMedCrossRefGoogle Scholar

2. 4.

Butera RJ Jr, Rinzel J, Smith JC (1999) Models of respiratory rhythm generation


in the pre-Bötzinger complex. I. Bursting pacemaker neurons. J Neurophysiol
82:382–397PubMedGoogle Scholar
3. 5.

Butera RJ Jr, Rinzel J, Smith JC (1999b) Models of respiratory rhythm


generation in the pre-Botzinger complex. II. Populations Of coupled pacemaker
neurons. J Neurophysiol 82:398–415Google Scholar

4. 6.

Cohen MI (1979) Neurogenesis of respiratory rhythm in the mammal. Physiol


Rev 59:1105–1173PubMedGoogle Scholar

5. 7.

Del Negro CA, Johnson SM, Butera RJ, Smith JC (2001) Models of respiratory
rhythm generation in the pre-Botzinger complex. III. Experimental tests of
model predictions. J Neurophysiol 86:59–74PubMedGoogle Scholar

6. 8.

De Troyer A, Kirkwood PA, Wilson TA (2004) Respiratory action of the


intercostals muscles. Physiol Rev 86:717–756Google Scholar

7. 9.

Ezure K (1990) Synaptic connections between medullary respiratory neurons


and considerations on the genesis of the respiratory rhythm. Prog Neurobiol
35:429–450PubMedCrossRefGoogle Scholar

8. 10.

Feldman JL (1986) Neurophysiology of breathing in mammals. In: Handbook of


physiology. The nervous system. intrinsic regulatory system in the brain. Am
Physiol Soc, Sect. 1, vol. IV, Chap. 9. Washington, DC, pp 463–524Google
Scholar

9. 11.

Feldman JL, McCrimmon DR (2003) Neural control of breathing. In: Squire LR,
Bloom FE, McConnell SK, Roberts JL, Spitzer NC, Zigmond MJ (eds)
Fundamental neuroscience, 2nd edn, Chap. 37. Academic, AmsterdamGoogle
Scholar

10. 12.

Feldman JL, Mitchell GG, Nattie EE (2003) Breathing: rhythmicity, plasticity,


chemosensitivity. Annu Rev Neurosci 26:239–266PubMedCrossRefGoogle
Scholar
11. 13.

Greer JJ, Funk GD, Ballanyi K (2005) Preparing for the first breath; prenatal
maturation of respiratory neural control. J Physiol 570:437–
444PubMedCrossRefGoogle Scholar

12. 14.

Haji A, Takeda R, Okazaki M (2000) Neuropharmacology of control of


respiratory rhythm and pattern in mature mammals. Pharmacol Ther 86:277–
304PubMedCrossRefGoogle Scholar

13. 15.

Klages S, Bellingham MC, Richter DW (1993) Late expiratory inhibition of stage


2 expiratory neurons in the cat – a correlate of expiratory termination. J
Neurophysiol 70:1307–1315PubMedGoogle Scholar

14. 16.

Long S, Duffin J (1986) The neuronal determinants of respiratory rhythm. Prog


Neurobiol 27:101–182PubMedCrossRefGoogle Scholar

15. 17.

Monteau, R, Hilaire G (1991) Spinal respiratory motoneurons. Prog Neurobiol


37:144–191CrossRefGoogle Scholar

16. 18.

Nattie EE (2001) Central chemosensitivity, sleep and wakefulness. Respiration


Physiology and Neurobiology 129:257–268Google Scholar

17. 19.

Netter FH (1997) Atlas of Human Anatomy, 2nd Edition. In: Dalley AE (ed)
Novartis, Hanover, NJ. p. 523 pp. 967–990Google Scholar

18. 20.

Ono K, Shiba K, Nakazawa K, Shimoyama I (2006) Synaptic origin of the


respiratory-modulated activity of laryngeal motoneurons. Neuroscience
140:1079–1088PubMedCrossRefGoogle Scholar

19. 21.

Pierrefiche O, Shevtsova NA, St-John WM, Paton JF, Rybak IA (2004) Ionic
currents and endogenous rhythm generation in the pre-Botzinger complex:
modelling and in vitro studies. Advances in Experimental Medicine and Biology
551:121–6PubMedCrossRefGoogle Scholar

20. 22.

Purvis LK, Smith JC, Koizumi H, Butera RJ (2007) Intrinsic bursters increase
the robustness of rhythm generation in an excitatory network. Journal of
Neurophysiology 97:1515–26PubMedCrossRefGoogle Scholar

21. 23.

Ramirez JM, Viemari JC (2005) Determinants of inspiratory activity.


Respiration Physiology and Neurobiology 147:145–157CrossRefGoogle Scholar

22. 24.

Richerson GB, Boron WF (2005) Control of ventilation. In: Medical Physiology.


WF Boron and EL Boulpaep (eds) Philadelphia, Elsevier Saunders, chapter 31,
pp. 712–734Google Scholar

23. 25.

Ritchter DW (1996) Neural regulation of respiration: Rhythmogenesis and


afferent control. In: Comprehensive Human Physiology. R. Gregor and U.
Windhorst (eds) Berlin, Springer, vol. 2, chapt. 105, pp. 2079–2095Google
Scholar

24. 26.

Richter DW, Ballanyi K, Schwarzacher S (1992) Mechanisms of respiratory


rhythm generation. Current Opinions in Neurobiology 26:788–
93CrossRefGoogle Scholar

25. 27.

Richter DW, Ballantyne D (1988) On the significance of post-inspiration.


Funtonanalyse biologischer Systeme 18:149–156Google Scholar

26. 28.

Richter DW, Pierrefiche O, Lalley PM, Polder HR (1996) Voltage-clamp analysis


of neurons within deep layers of the brain. Journal of Neuroscience Methods
67:121–131PubMedCrossRefGoogle Scholar

27. 29.
Richter DW, Spyer KM (2001) Studying rhythmogenesis of breathing:
comparison of in vivo and in vitro models. Trends in Neuroscience 24:464–
472CrossRefGoogle Scholar

28. 30.

Rybak IA, Shevtsova NA, Paton JF, Dick TE, St.-John WM, Morschel M.,
Dutschmann M (2004a) Modeling the ponto-medullary respiratory network.
Resp. Physiol. Neurobiol 143:307–319CrossRefGoogle Scholar

29. 31.

Rybak IA, Shevtsova NA, Paton JF, Pierrefiche O, St-John WM, Haji A (2004b)
Modelling respiratory rhythmogenesis: focus on phase switching mechanisms.
Advances in Experimental Medicine and Biology 551:189–94Google Scholar

30. 32.

Shao XM, Feldman JL (2005) Cholinergic neurotransmission in PreBötzinger


Complex modulates excitability of respiratory neurons and regulates respiratory
rhythm. Neuroscience 130:1069–1081PubMedCrossRefGoogle Scholar

31. 33.

Smith JC, Butera RJ, Koshiya N, Del Negro C, Wilson CG, Johnson SM (2000)
Respiratory rhythm generation in neonatal and adult mammals: the hybrid
pacemaker-network model. Respiration Physiology 122:131–
47PubMedCrossRefGoogle Scholar

32. 34.

Tian GF, Duffin J (1996) Connections from upper cervical inspiratory neurons to
phrenic and intercostal motoneurons studies with cross-correlation in the
decerebrate rat. Experimental Brain Research 110:196–204CrossRefGoogle
Scholar

33. 35.

Wood PG, Daniels CB, Orgeig S (1995) Functional significance and control of
release of pulmonary surfactant in the lizard lung. American Journal of
Physiology, Regulatory, Integrative and Comparative Physiology 269:R838–
R847Google Scholar

You might also like