[Effect of captopril on hypoxia-induced pulmonary hypertension in pigs]

The role of angiotensin system in the development of hypoxic pulmonary hypertension, in nine pigs (50 +/- 8 kg) were studied. A Swan-Ganz Catheter and an arterial catheter were inserted into the pulmonary artery and aorta, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), Cardiac output (CO) and arterial blood gases were monitored before and after hypoxia and captopril injection (7.3 mg/kg.iv). Plasma renin activity (PRA) and angiotensin II (AT-II) were measured by RIA. Angiotensin converting enzyme (ACE) was measured by fluorometry. Results showed that during hypoxemia (PaO2 6.3 +/- 0.2 kPa, PaCO2 5.4 +/- 0.2 kPa), PAP increased from 2.43 +/- 0.17 to 3.76 +/- 0.2 kPa, (P less than 0.05) and right ventricle stroke work index (BVSWI) from 55.7 +/- 7.2 to 91.3 +/- 9.3 mJ/m2 (P less than 0.05). PRA increased from 0.56 +/- 0.19 to 1.28 +/- 6.30 mol. L-1/h (P less than 0.02) and AT-II from 62.4 +/- 17.4 to 133.3 +/- 31.8 ng/L (P less than 0.01); but ACE decreased from 77.6 +/- 5.6 to 58.4 +/- 4.2 mumol.min-1/L (P less than 0.02). After Captopril injection ACE was reduced to 26.7 +/- 3.4 mumol.min-1/L (P less than 0.001) and AT-II dropped to 61.9 +/- 15.5 ng/L (P less than 0.01), as compared with those during hypoxemia. There was significant correlation between PAP and PRA (r = 0.5643 P less than 0.01). We surmise that angiotensin system may play a part in acute hypoxia-induced pulmonary hypertension, and captopril Inhibits AT-II, leading to the drop of pulmonary arterial pressure.