Angiotensin 11 Receptor Blockade and Effects on Pulmonary Hemodynamics and Hypoxic Pulmonary Vasoconstriction in Humans
| Autor: | Robert I. Cargill, Brian J. Lipworth, David G. Kiely |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Pulmonary and Respiratory Medicine
Angiotensin receptor Cardiac output business.industry Hypoxia (medical) Critical Care and Intensive Care Medicine Angiotensin II Hypoxemia chemistry.chemical_compound medicine.anatomical_structure chemistry Anesthesia Hypoxic pulmonary vasoconstriction Vascular resistance medicine medicine.symptom Cardiology and Cardiovascular Medicine business Saralasin |
| Zdroj: | Chest. 110:698-703 |
| ISSN: | 0012-3692 |
| DOI: | 10.1378/chest.110.3.698 |
| Popis: | Study objective We examined the hypothesis that angiotensin II (ANG II) is a modulator of pulmonary vascular tone by examining the effects of ANG II blockade on pulmonary hemodynamics during normoxemia and hypoxemia in normal volunteers with an activated renin angiotensin system (RAS). Participants and interventions Eight normal volunteers, pretreated with furosemide, were studied on two separate occasions and received either an infusion of saralasin, 5 µg/kg/min, or placebo. After 20 min, they were rendered hypoxemic, by breathing N 2 /O 2 mixture for 20 min to achieve arterial oxygen saturation (SaO 2 ) of 85 to 90% adjusted for a further 20 min to achieve SaO 2 of 75 to 80%. Doppler echocardiography was used to measure mean pulmonary artery pressure (MPAP), cardiac output, and hence total pulmonary vascular resistance (TPR). Results Saralasin compared with placebo resulted in a significant (p>0.05) reduction in MPAP during normoxemia, 6.70±1.0 vs 11.7±1.3 mm Hg; at SaO 2 of 85 to 90%, 14.7±1.4 vs 20.5±1.0 mm Hg; and at SaO 2 of 75 to 80%, 18.1±1.9 vs 27.8±1.9 mm Hg, respectively. Likewise saralasin compared with placebo resulted in a significant reduction in TPR during normoxemia, 104±14 vs 180±20 dyne·s·cm −5 ; at SaO 2 of 85 to 90%, 222±24 vs 295±21 dyne·s·cm −5 ; and at SaO 2 of 75 to 80%, 238±21 vs 362±11 dyne·s·cm −5 , respectively. The δM?α? response to hypoxemia was likewise significantly (p>0.01) attenuated by saralasin infusion compared with placebo: mean difference 5.0 mm Hg, 95% confidence interval (CI) 1.9 to 8.08, and there was a trend toward attenuation of the ATPR response to hypoxemia (0.05>p>0.10): mean difference 47 dyne·s·cm −5 , 95% CI, −10 to 105. Conclusion In addition to causing pulmonary vasodilatation in the presence of an activated RAS, our results suggest that ANG II receptor blockade attenuates acute hypoxic pulmonary vasoconstriction and that ANG II may play a role in modulating this response in normal man. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|