Dipartimento di Scienze Cliniche e Biologiche, dell'Università di Torino, Regione Gonzole 10, 10043 Orbassano (TO), Italy.
Basic Res Cardiol. 2010 Mar;105(2):181-92. doi: 10.1007/s00395-009-0075-6. Epub 2009 Dec 13.
Brief periods (a few seconds) of cyclic coronary occlusions applied early in reperfusion induce a cardioprotection against infarct size, called postconditioning (PostC) in which B(2)-bradykinin receptors play a pivotal role. Since angiotensin-converting enzyme (ACE) inhibitors reduce degradation of kinins, we studied the effects of PostC on infarct size and postischemic myocardial dysfunction in both normotensive (WKY) and spontaneously hypertensive rats (SHR) acutely or chronically treated with the ACE inhibitor Captopril. Isolated hearts from SHR and WKY rats were subjected to the following protocols: (a) ischemia for 30- and 120-min reperfusion (I/R); (b) I/R + PostC protocol (5-cycles 10-s I/R); (c) pretreatment with Captopril for 4-weeks before to subject the hearts to I/R with or without PostC maneuvers. Some SHR hearts were treated with Captopril during the 20- or 40-min early reperfusion with or without PostC maneuvers. Cardiac function was assessed in vivo with echocardiography. Left ventricular pressure and infarct size were measured ex vivo. Chronic Captopril significantly reduced left ventricular hypertrophy in SHR, and reduced infarct size in both WKY and SHR hearts. PostC maneuvers significantly reduced infarct size in WKY, but not in SHR hearts. Yet, PostC slightly improved postischemic systolic function in untreated SHR. Captopril given in reperfusion was unable to limit I/R injury in SHR hearts. Data show that PostC protection against infarct size is blunted in SHR and that PostC is unable to add its protective effect to those of chronic Captopril, which per se reduces cardiac hypertrophy and heart susceptibility to I/R insult.
短暂的（几秒钟）循环性冠状动脉闭塞应用于再灌注早期可诱导针对梗死面积的心脏保护作用，称为后处理（PostC），其中 B(2)-缓激肽受体发挥关键作用。由于血管紧张素转换酶（ACE）抑制剂可减少激肽的降解，我们研究了后处理对急性或慢性用 ACE 抑制剂卡托普利治疗的正常血压（WKY）和自发性高血压大鼠（SHR）的梗死面积和缺血后心肌功能障碍的影响。来自 SHR 和 WKY 大鼠的离体心脏接受了以下方案的处理：（a）缺血 30 分钟和 120 分钟再灌注（I/R）；（b）I/R + PostC 方案（5 个循环 10 秒 I/R）；（c）在将心脏暴露于 I/R 之前用卡托普利预处理 4 周，无论是否进行 PostC 操作。一些 SHR 心脏在 20 分钟或 40 分钟早期再灌注期间用或不用 PostC 操作用卡托普利处理。通过超声心动图在体内评估心脏功能。在体测量左心室压力和梗死面积。慢性卡托普利显著降低 SHR 的左心室肥厚，并降低 WKY 和 SHR 心脏的梗死面积。PostC 操作显著降低了 WKY 心脏的梗死面积，但对 SHR 心脏没有影响。然而，PostC 略微改善了未经处理的 SHR 的缺血后收缩功能。在 SHR 心脏中，再灌注时给予卡托普利无法限制 I/R 损伤。数据表明，PostC 对梗死面积的保护作用在 SHR 中减弱，PostC 无法将其保护作用添加到慢性卡托普利的作用中，慢性卡托普利本身可降低心脏肥大和对 I/R 损伤的敏感性。
