Schoelkens B A, Linz W
Hoechst AG, Frankfurt/Main, Germany.
Agents Actions Suppl. 1992;38 ( Pt 2):36-42.
Bradykinin perfusion (BK 1 x 10(-12) to 1 x 10(-8) mol/l) of isolated working rat hearts with postischemic reperfusion arrhythmias induced a reduction of the incidence as well as duration of ventricular fibrillation, improvement of cardiodynamics via increased left ventricular pressure, contractility, and coronary flow without changes in heart rate. These beneficial effects were accompanied by reduced activities of the cytosolic enzymes lactate dehydrogenase and creatine kinase as well as lactate output. In the myocardial tissue lactate content was reduced and the energy rich phosphates increased compared to saline perfused control hearts. Glycogen stores were also preserved. These beneficial effects of BK were concentration-dependently abolished by perfusion of the B2 kinin receptor antagonist HOE 140 and the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA). These results suggest that improved cardiac function during and after myocardial ischemia as well as increased energy rich phophates and glycogen stores are mediated by BK and the subsequent release of NO, shifting myocardial metabolism during ischemia and reperfusion to the glucose pathway which leads to changes indicative for cardioprotection.
用缓激肽灌注（1×10⁻¹²至1×10⁻⁸mol/L的缓激肽）诱发缺血后再灌注心律失常的离体工作大鼠心脏，可降低室颤的发生率和持续时间，通过增加左心室压力、收缩力和冠脉血流量改善心脏动力学，而心率无变化。这些有益作用伴随着胞质酶乳酸脱氢酶和肌酸激酶的活性降低以及乳酸输出减少。与生理盐水灌注的对照心脏相比，心肌组织中的乳酸含量降低，高能磷酸盐增加。糖原储备也得以保存。缓激肽的这些有益作用被B2激肽受体拮抗剂HOE 140和一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸（L-NNA）的灌注浓度依赖性地消除。这些结果表明，心肌缺血期间及之后心脏功能的改善以及高能磷酸盐和糖原储备的增加是由缓激肽及随后一氧化氮的释放介导的，在缺血和再灌注期间将心肌代谢转向葡萄糖途径，这导致了具有心脏保护作用的变化。
