The Heart Institute of Good Samaritan Hospital, Division of Cardiovascular Medicine of the Keck School of Medicine, University of Southern California, Los Angeles, CA 90017, USA.
Postgrad Med. 2011 Mar;123(2):49-55. doi: 10.3810/pgm.2011.03.2263.
Experimental and clinical studies have demonstrated that myocardial ischemia induces activation of various components of the renin-angiotensin system (RAS), including angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensins, and angiotensin receptors, in the acute phase of myocardial infarction and the postinfarction remodeling process. Pharmacological inhibition of the RAS by administration of renin inhibitors, ACE inhibitors, and angiotensin receptor blockers has shown beneficial effects on the pathological processes of myocardial infarction in both experimental animal studies and clinical trials. However, the potential mechanisms responsible for the cardioprotection of RAS inhibition remain unclear. In this review, we discuss roles of RAS blocking in the prevention of myocardial ischemia/reperfusion injury and postinfarction remodeling.
实验和临床研究表明，心肌缺血在心肌梗死急性期和梗死后重构过程中诱导肾素-血管紧张素系统（RAS）的各种成分激活，包括血管紧张素原、肾素、血管紧张素转换酶（ACE）、血管紧张素和血管紧张素受体。通过给予肾素抑制剂、ACE 抑制剂和血管紧张素受体阻滞剂来抑制 RAS 的药理学作用，在实验动物研究和临床试验中均显示对心肌梗死的病理过程有益。然而，RAS 抑制的心脏保护作用的潜在机制尚不清楚。在这篇综述中，我们讨论了 RAS 阻断在预防心肌缺血/再灌注损伤和梗死后重构中的作用。
