Jiang M
Peking Union Medical College Hospital, Beijing.
Zhonghua Xin Xue Guan Bing Za Zhi. 1991 Dec;19(6):342-4, 396.
A serial measurements of plasma renin activity (PRA), serum angiotensin converting enzyme activity (ACE), concentrations of plasma angiotensin II (AII) and plasma aldosterone (Ald) in 38 consecutive patients with acute myocardial infarction (AMI) or suspected AMI showed that PRA, AII and Ald levels increased in patients with AMI, especially within first week after onset, and were significantly higher in those cases with severe complications. ACE kept in normal range in all subjects. After small dose captopril therapy, ACE and Ald decreased significantly, PRA and AII increased in 6 patients with AMI. Small dose captopril could cause remarkable blood pressure reduction, but no effect on heart rate. The results suggested that renin-angiotensin-aldosterone system was activated during AMI, especially in cases with severe complications. Captopril could inhibit this system partially.
对38例连续的急性心肌梗死（AMI）或疑似AMI患者进行的血浆肾素活性（PRA）、血清血管紧张素转换酶活性（ACE）、血浆血管紧张素II（AII）浓度及血浆醛固酮（Ald）的系列测定显示，AMI患者的PRA、AII和Ald水平升高，尤其是在发病后的第一周内，且严重并发症患者的这些指标显著更高。所有受试者的ACE均保持在正常范围内。小剂量卡托普利治疗后，ACE和Ald显著降低，6例AMI患者的PRA和AII升高。小剂量卡托普利可显著降低血压，但对心率无影响。结果提示，AMI期间肾素-血管紧张素-醛固酮系统被激活，尤其是在严重并发症患者中。卡托普利可部分抑制该系统。
