Jederlinic P, Hill N S, Ou L C, Fanburg B L
Pulmonary Division, New England Medical Center, Boston.
Thorax. 1988 Sep;43(9):703-7. doi: 10.1136/thx.43.9.703.
The decrease in lung angiotensin converting enzyme (ACE) activity occurring in rats during chronic hypoxia might be related to the pulmonary haemodynamic response or to the hypoxia. A study in rats was carried out to investigate this question. Rats from the Hilltop (H) strain are known to develop more severe pulmonary hypertension as a result of chronic hypoxia than rats from the Madison (M) strain despite having virtually identical arterial and mixed venous oxygen tensions. Rats from H and M strains were exposed to hypoxia (0.5 atm) for 3-21 days and lung and serum ACE activities were determined. After three days' hypobaria lung ACE activity was significantly lower and serum ACE significantly higher in H than in M rats. Linear regressions for lung ACE activity and right ventricular:body weight ratios showed significant inverse correlations and were similar in the two strains. The results suggest that pulmonary hypertension and not hypoxia determines the reduction in lung ACE activity, possibly by releasing ACE into the blood stream.
慢性缺氧期间大鼠肺血管紧张素转换酶(ACE)活性的降低可能与肺血流动力学反应或缺氧有关。为研究此问题,对大鼠进行了一项研究。已知山顶(H)品系的大鼠由于慢性缺氧比麦迪逊(M)品系的大鼠发展出更严重的肺动脉高压,尽管它们的动脉血氧张力和混合静脉血氧张力几乎相同。将H和M品系的大鼠暴露于低氧(0.5个大气压)环境3至21天,并测定肺和血清ACE活性。低氧3天后,H品系大鼠的肺ACE活性显著低于M品系大鼠,而血清ACE则显著高于M品系大鼠。肺ACE活性与右心室重量比的线性回归显示出显著的负相关,且在两个品系中相似。结果表明,是肺动脉高压而非缺氧决定了肺ACE活性的降低,可能是通过将ACE释放到血流中实现的。