肾缺血预处理保护缺血再灌注损伤心肌的机制

目的:探讨心脏外脏器缺血预处理对心肌保护作用的机制。方法:将动物分为缺血／再灌注(I/R)、经典缺血预处理(CIPC)、肾缺血预处理(KIPC)及超氧化物歧化酶＋肾缺血预处理(SOD+KIPC)4组。比较各组心肌内源性保护物质一氧化氮(NO)含量、5'-核苷酸酶(5'-NT)活性的变化。结果:肾缺血预处理能明显改善左室功能,降低再灌性心律失常发生率及血浆磷脂酶A₂(PLA₂)活性,同时使心肌5'－NT活性、NO含量明显高于I/R组。而在肾缺血预处理前用超氧化物歧化酶处理则肾缺血预处理的心肌保护作用明显弱于KIPC组,与心肌5'－NT活性、NO含量下降相一致。结论:肾缺血预处理对心肌的保护作用可能也与通过调动心肌内源性保护物质的释放有关,氧自由基在介导该类物质的释放中起了重要的作用。

Mechanisms underlying the protective effect of renal ischemic preconditioning on ischemia-reperfusion myocardium of rabbits

AIM: To investigate the mechanisms underlying the protective effect of kidney ischemic preconditioning on rabbit myocardium in case of ischemia-reperfusion and the possible role of oxygen free radicals in the process. METHODS: Animals were divided into four groups: ischemia/reperfusion(I/R), classical ischemic preconditioning(CIPC), kidney ischemic preconditioning (KIPC) and superoxide dismutase in combination with kidney ischemic preconditioning(SOD KIPC). The endo genous myocardial pretective material, nitric oxide(NO) and 5'-nucleotidase(5'-NT) were checked in four groups. RESULTS: As compared with I/R group, both CIPC and KIPC could ameliorate left ventricular function, reduce plasma PLA 2 activity and arrhythogenic rate also, the myocardial 5'-NT and NO production were significantly higher than that of the rabbit of I/R group. However, the protective effect on rabbit myocardium was significantly weakened by the SOD administration before the ischemic preconditioning. CONCLUSION: Protective effect of KIPC on myocardium may be due to increase in endo genous myocardial protective materials, oxygen free radicals may play an important role in the endo genous myocardial protective material release.