Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfus... more Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. Prospective randomized animal study. University research laboratory. Adult male Wistar-Kyoto rats. The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.
University College Dublin, Dublin 4, Ireland, UCD Conway Institute of Biomolecular and Biomedical... more University College Dublin, Dublin 4, Ireland, UCD Conway Institute of Biomolecular and Biomedical Sciences, Dublin 4, Ireland, 1 2 ... Cambridge University, Cambridge, United Kingdom, University of Cambridge, Cambridge, United Kingdom ... Corresponding author's email: ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Angiogenesis And Vascular ...
Chronic hypoxic pulmonary hypertension is characterized by a sustained increase in pulmonary arte... more Chronic hypoxic pulmonary hypertension is characterized by a sustained increase in pulmonary arterial pressure due to abnormally elevated pulmonary vascular resistance. This increased vascular resistance was previously thought to be due largely to changes in the structure of the pulmonary vasculature, i.e. lumen narrowing due to wall hypertrophy and loss of vessels. Recently, this model has been challenged by the demonstration that hypoxic pulmonary hypertension in the rat is caused almost completely by sustained vasoconstriction. The contribution of this vasocontriction to hypoxic pulmonary hypertension has not been examined directly in other species. We exposed groups of mice to hypoxia (10% O(2)) or normoxia for 3 weeks, following which the lungs were removed post mortem, and vascular resistance was measured in an isolated, ventilated, perfused preparation. Mean pulmonary vascular resistance was significantly increased in hypoxic compared with control normoxic lungs. The rho kinase inhibitor Y27635 (10(-4)m) (Tocris Bioscience, Bristol, United Kingdom.) significantly reduced the mean (± SEM) hypoxia induced increase by 45.4 (10.8)%, implying that structural vascular changes acounted for the remainder of the hypoxic increase. Stereological quantification showed a significant reduction in the mean lumen diameter of the fully relaxed vessels in hypoxic lungs compared with normoxic control lungs; there was no intra-acinar vessel loss. Thus, in contrast to the rat, hypoxic pulmonary hypertension in the mouse is due to two mechanisms contributing equally: sustained vasoconstriction and structural lumen narrowing of intra-acinar vessels. These important species diferences must be considered when using genetically mutated mice to investigate the mechanisms underlying pulmonary hypertension.
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. T... more Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. The balance between transforming growth factor β1 and bone morphogenetic protein (BMP) signaling plays an important role in tissue homeostasis, and alterations can result in pulmonary fibrosis. We hypothesized that multiple BMP accessory proteins may be responsible for maintaining this balance in the lung. Using the bleomycin mouse model for fibrosis, we examined an array of BMP accessory proteins for changes in mRNA expression. We report significant increases in mRNA expression of gremlin 1, noggin, follistatin, and follistatin-like 1 (Fstl1), and significant decreases in mRNA expression of chordin, kielin/chordin-like protein, nephroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI). Protein expression studies demonstrated increased levels of noggin, BAMBI, and FSTL1 in the lungs of bleomycin-treated mice and in the lungs of idiopathic pulmonary fibrosis patients. Furthermore, we demonstrated that transforming growth factor β stimulation resulted in increased expression of noggin, BAMBI, and FSTL1 in human small airway epithelial cells. These results provide the first evidence that multiple BMP accessory proteins are altered in fibrosis and may play a role in promoting fibrotic injury.
Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. T... more Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. The balance between transforming growth factor β1 and bone morphogenetic protein (BMP) signaling plays an important role in tissue homeostasis, and alterations can result in pulmonary fibrosis. We hypothesized that multiple BMP accessory proteins may be responsible for maintaining this balance in the lung. Using the bleomycin mouse model for fibrosis, we examined an array of BMP accessory proteins for changes in mRNA expression. We report significant increases in mRNA expression of gremlin 1, noggin, follistatin, and follistatin-like 1 (Fstl1), and significant decreases in mRNA expression of chordin, kielin/chordin-like protein, nephroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI). Protein expression studies demonstrated increased levels of noggin, BAMBI, and FSTL1 in the lungs of bleomycin-treated mice and in the lungs of idiopathic pulmonary fibrosis patients. Furthermore, we demonstrated that transforming growth factor β stimulation resulted in increased expression of noggin, BAMBI, and FSTL1 in human small airway epithelial cells. These results provide the first evidence that multiple BMP accessory proteins are altered in fibrosis and may play a role in promoting fibrotic injury.
American Journal of Physiology Lung Cellular and Molecular Physiology, Sep 1, 1999
We hypothesized that abnormal ventilation-perfusion matching in chronically infected lungs was in... more We hypothesized that abnormal ventilation-perfusion matching in chronically infected lungs was in part due to excess nitric oxide (NO) production after upregulation of inducible NO synthase (iNOS) expression. Rats were anesthetized and inoculated intratracheally with Pseudomonas aeruginosa incorporated into agar beads (chronically infected) or with sterile agar beads (placebo inoculated) and killed 10-15 days later. Immunohistochemistry demonstrated increased expression of iNOS and reduced expression of endothelial NOS (eNOS) in chronically infected compared with placebo-inoculated or noninoculated lungs. In isolated lungs from chronically infected rats, NOS inhibition with N(omega)-nitro-L-arginine methyl ester increased the mean perfusion pressure (14.4 +/- 2.7 mmHg) significantly more than in the placebo-inoculated (4.8 +/- 1.0 mmHg) or noninoculated (5.3 +/- 0.8 mmHg) lungs (P < 0.01). Although the chronically infected lungs were more sensitive to NOS inhibition, further evidence suggested that the increased iNOS expression was not associated with enhanced iNOS activity. Selective inhibitors of iNOS did not produce an increase in vascular resistance similar to that produced by nonselective inhibitors. Accumulation of nitrate/nitrite in the perfusate of isolated lungs was unchanged by chronic infection. Thus although iNOS expression was increased in chronic pulmonary infection, iNOS activity in the intact lung was not. Nonetheless, endogenous NO production was essential to maintain normal vascular resistance in these lungs.
C61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS II, 2011
Page 1. / Thematic Poster Session / Tuesday, May 17/8:15 AM-4:30 PM C61 PULMONARY HYPERTENSION: E... more Page 1. / Thematic Poster Session / Tuesday, May 17/8:15 AM-4:30 PM C61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS II / Area H, Hall B (Upper Level), Colorado Convention Center The Role Of Placental ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
Evolving and changing undergraduate medical curricula raise concerns that there will no longer be... more Evolving and changing undergraduate medical curricula raise concerns that there will no longer be a place for basic sciences. National and international trends show that 5-year programmes with a pre-requisite for school chemistry are growing more prevalent. National reports in Ireland show a decline in the availability of school chemistry and physics. This observational cohort study considers if the basic sciences of physics, chemistry and biology should be a prerequisite to entering medical school, be part of the core medical curriculum or if they have a place in the practice of medicine. Comparisons of means, correlation and linear regression analysis assessed the degree of association between predictors (school and university basic sciences) and outcomes (year and degree GPA) for entrants to a 6-year Irish medical programme between 2006 and 2009 (n = 352). We found no statistically significant difference in medical programme performance between students with/without prior basic s...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center A Role For The Cxcl12/cxcr7/cxcr4 Axis In Pulmonary Hypertension ...
The purpose of the study was to determine the effects of early plasmin-mediated digests of rat fi... more The purpose of the study was to determine the effects of early plasmin-mediated digests of rat fibrinogen on the vascular tone of rat pulmonary artery in order to compare with reported vasoactive effects of high levels of isolated human peptides in various rat vascular beds. Isometric tension was monitored in isolated rings of rat pulmonary artery precontracted with phenylephrine (4×10−8mol).
... 1 School of Medicine and Medical Science Conway Institute University College Dublin, Ireland ... more ... 1 School of Medicine and Medical Science Conway Institute University College Dublin, Ireland e-mail: paul.mcloughlin{at}ucd.ie 2 Department of Pharmacology and Center for Lung Biology University ... Clin Sci (Lond) 61: 569–580, 1981.[Medline]; Finlay M, Barer GR, Suggett AJ. ...
Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfus... more Deliberate induction of hypercapnic acidosis protects against lung injury after ischemia-reperfusion, endotoxin-induced, and ventilation-induced lung injury. The efficacy of hypercapnic acidosis in bacterial lung infection, a common cause of acute respiratory distress syndrome, is not known. Furthermore, its effect may differ depending on the presence or absence of antibiotic therapy. We investigated whether hypercapnic acidosis-induced by adding CO2 to inspired gas-would protect against acute lung injury induced by pulmonary Escherichia coli instillation in an in vivo model in the presence and absence of effective antibiotic therapy. Prospective randomized animal study. University research laboratory. Adult male Wistar-Kyoto rats. The animals were anesthetized and ventilated. In series 1, rats were administered intravenous ceftriaxone (100 mg x kg) and randomized to normocapnia (Normocapnia-ABx; Fico2 0.00, n = 10) or hypercapnia (Hypercapnia-ABx; Fico2 0.05, n = 10) groups. E. coli (8.4 x 10 colony forming units) was instilled intratracheally. Series 2 animals did not receive antibiotics. They were randomized to normocapnia (Normocapnia, n = 10) or hypercapnia (Hypercapnia, n = 10) groups, and intratracheal E. coli was administered. All animals were ventilated for 6 hrs. In series 1, there were no differences between Hypercapnia-ABx and Normocapnia-ABx groups with regard to: (a-a)o2 gradient (mean +/- sem; 215 +/- 13 vs. 252 +/- 22 mm Hg), Pao2, bronchoalveolar lavage neutrophil count, static lung compliance, or histologic injury. Lung bacterial yield was not different between the groups. In series 2, in the absence of antibiotic therapy, there were no differences between Hypercapnia and Normocapnia groups in: (a-a)o2 gradient (mean +/- sem, 345 +/- 25 vs. 332 +/- 23 mm Hg), systemic Pao2, bronchoalveolar lavage neutrophil count, or static lung compliance. Lung bacterial yield was not altered by hypercapnia in either series 1 or 2. We conclude that hypercapnic acidosis did not alter the magnitude of the lung injury induced by intratracheal E. coli instillation in the presence or absence of antibiotics.
University College Dublin, Dublin 4, Ireland, UCD Conway Institute of Biomolecular and Biomedical... more University College Dublin, Dublin 4, Ireland, UCD Conway Institute of Biomolecular and Biomedical Sciences, Dublin 4, Ireland, 1 2 ... Cambridge University, Cambridge, United Kingdom, University of Cambridge, Cambridge, United Kingdom ... Corresponding author's email: ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Angiogenesis And Vascular ...
Chronic hypoxic pulmonary hypertension is characterized by a sustained increase in pulmonary arte... more Chronic hypoxic pulmonary hypertension is characterized by a sustained increase in pulmonary arterial pressure due to abnormally elevated pulmonary vascular resistance. This increased vascular resistance was previously thought to be due largely to changes in the structure of the pulmonary vasculature, i.e. lumen narrowing due to wall hypertrophy and loss of vessels. Recently, this model has been challenged by the demonstration that hypoxic pulmonary hypertension in the rat is caused almost completely by sustained vasoconstriction. The contribution of this vasocontriction to hypoxic pulmonary hypertension has not been examined directly in other species. We exposed groups of mice to hypoxia (10% O(2)) or normoxia for 3 weeks, following which the lungs were removed post mortem, and vascular resistance was measured in an isolated, ventilated, perfused preparation. Mean pulmonary vascular resistance was significantly increased in hypoxic compared with control normoxic lungs. The rho kinase inhibitor Y27635 (10(-4)m) (Tocris Bioscience, Bristol, United Kingdom.) significantly reduced the mean (± SEM) hypoxia induced increase by 45.4 (10.8)%, implying that structural vascular changes acounted for the remainder of the hypoxic increase. Stereological quantification showed a significant reduction in the mean lumen diameter of the fully relaxed vessels in hypoxic lungs compared with normoxic control lungs; there was no intra-acinar vessel loss. Thus, in contrast to the rat, hypoxic pulmonary hypertension in the mouse is due to two mechanisms contributing equally: sustained vasoconstriction and structural lumen narrowing of intra-acinar vessels. These important species diferences must be considered when using genetically mutated mice to investigate the mechanisms underlying pulmonary hypertension.
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. T... more Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. The balance between transforming growth factor β1 and bone morphogenetic protein (BMP) signaling plays an important role in tissue homeostasis, and alterations can result in pulmonary fibrosis. We hypothesized that multiple BMP accessory proteins may be responsible for maintaining this balance in the lung. Using the bleomycin mouse model for fibrosis, we examined an array of BMP accessory proteins for changes in mRNA expression. We report significant increases in mRNA expression of gremlin 1, noggin, follistatin, and follistatin-like 1 (Fstl1), and significant decreases in mRNA expression of chordin, kielin/chordin-like protein, nephroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI). Protein expression studies demonstrated increased levels of noggin, BAMBI, and FSTL1 in the lungs of bleomycin-treated mice and in the lungs of idiopathic pulmonary fibrosis patients. Furthermore, we demonstrated that transforming growth factor β stimulation resulted in increased expression of noggin, BAMBI, and FSTL1 in human small airway epithelial cells. These results provide the first evidence that multiple BMP accessory proteins are altered in fibrosis and may play a role in promoting fibrotic injury.
Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. T... more Idiopathic pulmonary fibrosis is a chronic, progressive fibrotic disease with a poor prognosis. The balance between transforming growth factor β1 and bone morphogenetic protein (BMP) signaling plays an important role in tissue homeostasis, and alterations can result in pulmonary fibrosis. We hypothesized that multiple BMP accessory proteins may be responsible for maintaining this balance in the lung. Using the bleomycin mouse model for fibrosis, we examined an array of BMP accessory proteins for changes in mRNA expression. We report significant increases in mRNA expression of gremlin 1, noggin, follistatin, and follistatin-like 1 (Fstl1), and significant decreases in mRNA expression of chordin, kielin/chordin-like protein, nephroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI). Protein expression studies demonstrated increased levels of noggin, BAMBI, and FSTL1 in the lungs of bleomycin-treated mice and in the lungs of idiopathic pulmonary fibrosis patients. Furthermore, we demonstrated that transforming growth factor β stimulation resulted in increased expression of noggin, BAMBI, and FSTL1 in human small airway epithelial cells. These results provide the first evidence that multiple BMP accessory proteins are altered in fibrosis and may play a role in promoting fibrotic injury.
American Journal of Physiology Lung Cellular and Molecular Physiology, Sep 1, 1999
We hypothesized that abnormal ventilation-perfusion matching in chronically infected lungs was in... more We hypothesized that abnormal ventilation-perfusion matching in chronically infected lungs was in part due to excess nitric oxide (NO) production after upregulation of inducible NO synthase (iNOS) expression. Rats were anesthetized and inoculated intratracheally with Pseudomonas aeruginosa incorporated into agar beads (chronically infected) or with sterile agar beads (placebo inoculated) and killed 10-15 days later. Immunohistochemistry demonstrated increased expression of iNOS and reduced expression of endothelial NOS (eNOS) in chronically infected compared with placebo-inoculated or noninoculated lungs. In isolated lungs from chronically infected rats, NOS inhibition with N(omega)-nitro-L-arginine methyl ester increased the mean perfusion pressure (14.4 +/- 2.7 mmHg) significantly more than in the placebo-inoculated (4.8 +/- 1.0 mmHg) or noninoculated (5.3 +/- 0.8 mmHg) lungs (P < 0.01). Although the chronically infected lungs were more sensitive to NOS inhibition, further evidence suggested that the increased iNOS expression was not associated with enhanced iNOS activity. Selective inhibitors of iNOS did not produce an increase in vascular resistance similar to that produced by nonselective inhibitors. Accumulation of nitrate/nitrite in the perfusate of isolated lungs was unchanged by chronic infection. Thus although iNOS expression was increased in chronic pulmonary infection, iNOS activity in the intact lung was not. Nonetheless, endogenous NO production was essential to maintain normal vascular resistance in these lungs.
C61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS II, 2011
Page 1. / Thematic Poster Session / Tuesday, May 17/8:15 AM-4:30 PM C61 PULMONARY HYPERTENSION: E... more Page 1. / Thematic Poster Session / Tuesday, May 17/8:15 AM-4:30 PM C61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS II / Area H, Hall B (Upper Level), Colorado Convention Center The Role Of Placental ...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center Hypoxic Upregulation Of ...
Evolving and changing undergraduate medical curricula raise concerns that there will no longer be... more Evolving and changing undergraduate medical curricula raise concerns that there will no longer be a place for basic sciences. National and international trends show that 5-year programmes with a pre-requisite for school chemistry are growing more prevalent. National reports in Ireland show a decline in the availability of school chemistry and physics. This observational cohort study considers if the basic sciences of physics, chemistry and biology should be a prerequisite to entering medical school, be part of the core medical curriculum or if they have a place in the practice of medicine. Comparisons of means, correlation and linear regression analysis assessed the degree of association between predictors (school and university basic sciences) and outcomes (year and degree GPA) for entrants to a 6-year Irish medical programme between 2006 and 2009 (n = 352). We found no statistically significant difference in medical programme performance between students with/without prior basic s...
B61. PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I, 2011
Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: ... more Page 1. / Thematic Poster Session / Monday, May 16/8:15 AM-4:30 PM / B61 PULMONARY HYPERTENSION: EXPERIMENTAL MODELS I Area A, Hall B (Upper Level), Colorado Convention Center A Role For The Cxcl12/cxcr7/cxcr4 Axis In Pulmonary Hypertension ...
The purpose of the study was to determine the effects of early plasmin-mediated digests of rat fi... more The purpose of the study was to determine the effects of early plasmin-mediated digests of rat fibrinogen on the vascular tone of rat pulmonary artery in order to compare with reported vasoactive effects of high levels of isolated human peptides in various rat vascular beds. Isometric tension was monitored in isolated rings of rat pulmonary artery precontracted with phenylephrine (4×10−8mol).
... 1 School of Medicine and Medical Science Conway Institute University College Dublin, Ireland ... more ... 1 School of Medicine and Medical Science Conway Institute University College Dublin, Ireland e-mail: paul.mcloughlin{at}ucd.ie 2 Department of Pharmacology and Center for Lung Biology University ... Clin Sci (Lond) 61: 569–580, 1981.[Medline]; Finlay M, Barer GR, Suggett AJ. ...
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