缺血后处理抑制氧化应激减轻家兔缺血再灌注心肌损伤

目的研究缺血后处理对缺血再灌注家兔心功能、体内丙二醛（MDA）含量及超氧化物歧化酶（S01））活性的影响。方法18只家免随机分为对照组、缺血预处理组和缺血后处理组（每组6只）。监测家兔缺血及再灌注时左室内压峰值（LVSP）、±dp／dtmax和再灌注后血清中MDA含量及SOD活力。结果与对照组比较．缺血预处理组及缺血后处理组LVSP及左室±dp／dtmax再灌注后的恢复率均高于对照组（P〈0．01）,血清MDA含量明显低于对照组（P〈0．05），SOD活力明显高于对照组（P〈0．05）。结论结果表明缺血后处理与通过抑制氧化应激能减轻家兔心肌缺血-再灌注损伤。

Ischemic Post-conditioning Attenuates Myocardial Ischemia Reperfusion Injury Through Inhibiting Oxidative Stress in Rabbits

Objective： To investigate the impact of ischemic preconditioning and ischemic postconditioning on cardiac function, malondialdehyde （MDA） and superoxide dismutase（SOD） during heart ischemia/reperfusion injury in rabbits. Methods：Eighteen rabbits were randomly divided into 3 groups （n ： 6 each）： control group,ischemic preconditioning group and ischemic postconditioning group. Left ventricular systolic pressure （LVSP）, ±dp/dtmax of the heart during reperfusion were determined, Ptasma MDA content and SOD activity were also measured. Re- suits ： Compared with those of control, LVSP and ~ dp/dtmax of the heart were better recovered during reperfusion in both of the conditioned groups（ P〈0.01）. The MDA concentrations in plasma in both of the conditioned groups were significantly lower than those in the control group （P〈0.05） and the SOD activities in plasma were significantly higher than those in the control group （P〈0.05）. Conclusion： The results demonstrate that ischemic post- conditioning, like ischemic preconditioning, improve cardiofunction, depresses the production of oxygen free radicals and attenuate reperfusion injury in ischemic heart.