Beneficial effects of bradykinin on myocardial energy metabolism and infarct size
Beneficial effects of bradykinin on myocardial energy metabolism and infarct size
复制标题
DOI：
10.1016/s0002-9149(97)00466-9
复制
发表时间：
1997-08-04
影响因子：
2.8
通讯作者：
Scholkens, BA
中科院分区：
文献类型：
--
作者：
Linz, W;Wiemer, G;Scholkens, BA
越来越多的证据表明心脏中存在局部激肽释放酶-激肽系统，在缺血心脏中，激肽的产生和释放的增强似乎具有心脏保护作用，在具有缺血-再灌注损伤的离体大鼠心脏中，用缓激肽灌注减少室颤的持续时间和发生率，改善心脏动力学，减少细胞溶质酶的释放，并保存富含能量的磷酸盐和糖原储存，在麻醉的动物中，冠状动脉内输注缓激肽后可产生类似的有益变化并限制梗死面积。抑制缓激肽和相关肽的分解可诱导类似的有益心脏效应。血管紧张素转换酶（ACE）抑制剂如雷米普利可增加心肌激肽，减少离体大鼠心脏缺血后再灌注损伤，并可分别减少梗死后动物的梗死面积和重构。阻断B-2激肽受体可增加缺血诱导的效应。在离体心脏中，缺血-再灌注损伤在B-2激肽受体拮抗剂艾替班特作用下加剧，这也消除了ACE抑制剂和外源性缓激肽的心脏保护作用，麻醉动物中ACE抑制剂和缓激肽引起的血管体积减小被艾替班特逆转。激肽有助于与缺血预处理相关的心脏保护作用。预处理缓激肽诱导的抗心肌梗死和梗死面积限制作用被艾替班特减弱。(C)1997年，Excerpta Medica，Inc.
There is growing evidence for a local kallikrein-kinin system in the heart, In the ischemic heart the enhanced generation and release of kinins seem to have cardioprotective actions, In isolated rat hearts with ischemia-reperfusion injuries, perfusion with bradykinin reduces the duration and incidence of ventricular fibrillations, improves cardiodynamics, reduces release of cytosolic enzymes, and preserves energy-rich phosphates and glycogen stores, In anesthetized animals, intracoronary infusion of bradykinin is followed by comparable beneficial changes and limits infarct size, Inhibition of breakdown of bradykinin and related peptides induces similar beneficial cardiac effects. Treatment with angiotensin-converting enzyme (ACE) inhibitors such as ramipril increases cardiac kinins and reduces postischemic reperfusion injuries in isolated rat hearts as well as infarct size and remodeling in postinfarcted animals, respectively, Blockade of B-2 kinin receptors increases ischemia-induced effects. In isolated hearts, ischemia-reperfusion injuries intensify with the B-2 kinin receptor antagonist icatibant, which also abolishes the cardioprotective effects of ACE inhibitors and of exogenous bradykinin, Infarct size reduction by ACE inhibitors and bradykinin in anesthetized animals is reversed by icatibant. Kinins contribute to the cardioprotective effects associated with ischemic preconditioning. Preconditioning of bradykinin-induced antiarrhythmic and infarct size-limiting effects are attenuated by icatibant. (C) 1997 by Excerpta Medica, Inc.