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目的：探讨内皮细胞损伤及功能变化在心肌缺血再灌注损伤中的发病机制及卡托普利对其的影响。方法：实验兔分为心肌缺血再灌注组（ｎ＝８），心肌缺血再灌注＋卡托普利治疗组（ｎ＝８）及假手术对照组（ｎ＝８）；分别测结扎前，缺血０．５小时，再灌注０．５小时、１．５小时和６小时共５个时相点。用放射免疫法测定血浆内皮素（ＥＴ），紫外分光光度计测一氧化氮（ＮＯ），Ｐｅｒｃｏｌ密度梯度离心法分离血循环内皮细胞。结果：心肌缺血０．５小时，血中ＥＴ、ＮＯ含量无明显变化，于再灌注０．５小时ＮＯ下降、ＥＴ升高，尤以再灌注１．５小时和６小时变化显著（Ｐ均＜０．０５）。循环内皮细胞则以再灌注１．５小时明显增高（Ｐ＜０．０５）。卡托普利可逆转上述指标。结论：再灌注导致内皮功能紊乱，进而加重内皮细胞损伤，二者互为因果关系，卡托普利通过保护内皮而减轻再灌注损伤。
OBJECTIVE: To investigate the pathogenesis of endothelial cell injury and functional changes during myocardial ischemia-reperfusion injury and the effects of captopril on it. Methods: The experimental rabbits were divided into three groups: ischemia reperfusion group (n = 8), myocardial ischemia reperfusion + captopril treatment group (n = 8) and sham operation control group , 0.5 hour ischemia, 0.5 hour reperfusion, 1.5 hours and 6 hours a total of 5 points. The plasma endothelin (ET) was measured by radioimmunoassay, the nitric oxide (NO) was measured by UV spectrophotometer, and the endothelial cells were separated by Percol density gradient centrifugation. Results: There was no significant change of ET and NO in the blood at 0.5 hour after myocardial ischemia, NO decreased at 0.5 hour after reperfusion, ET increased, especially at 1.5 hours and 6 hours after reperfusion <0.05). Circulating endothelial cells were significantly increased after 1.5 hours of reperfusion (P <0.05). Captopril can reverse the above indicators. CONCLUSION: Reperfusion leads to endothelial dysfunction, which in turn aggravates endothelial cell injury. Mutual causality between the two is that captopril reduces reperfusion injury by protecting the endothelium.