Szidon P, Bairey N, Oparil S
Circ Res. 1980 Feb;46(2):221-6. doi: 10.1161/01.res.46.2.221.
We studied the effect of acute hypoxia on pulmonary conversion of angiotensin I to II in anesthetized dogs. When arterial PO2 was decreased from 86 +/- 14 (SD) to 33 +/- 8 mm Hg without changing pH or PCO2, the single passage conversion of intravenous boluses of radiolabeled angiotensin I in tracer doses fell significantly (P less than 0.005) from 72 +/- 4 to 67 +/- 6%. The effect of comparable levels of hypoxemia on the conversion of continuous intravenous infusions of pharmacological doses (1000 times physiological) of angiotensin I was greater: from 55 +/- 14 to 33 +/- 13% (P less than 0.025). There was prompt return of percent conversion ratios to control levels when hypoxemia was reversed. We conclude that acute hypoxia is associated with a reversible decrease in pulmonary angiotensin converting enzyme availability.
我们研究了急性低氧对麻醉犬肺脏将血管紧张素I转化为血管紧张素II的影响。当动脉血氧分压从86±14(标准差)毫米汞柱降至33±8毫米汞柱,而pH值和二氧化碳分压不变时,静脉注射微量放射性标记血管紧张素I的单次通过转化率显著下降(P<0.005),从72±4%降至67±6%。同等程度的低氧血症对静脉持续输注药理剂量(生理剂量的1000倍)血管紧张素I转化率的影响更大:从55±14%降至33±13%(P<0.025)。当低氧血症得到纠正时,转化率百分比迅速恢复到对照水平。我们得出结论,急性低氧与肺血管紧张素转换酶活性的可逆性降低有关。