氢气对大鼠离体心肌缺血再灌注损伤的保护作用及机制

摘要

Objective To explore the protective effects of hydrogen saturated saline in induced myocardial ischemia reperfusion injury in rats .Methods Forty-eight rats were divided randomly into the experimental group (24) and the con-trol group (24).The rats of experimental group were treated with K-R solution combined with hydrogen saturated saline , the controls were given K-R solution only .After the treatment , the hearts were excised rats and Langendorff model .And the heart of the in vitro by inverse perfusion for 10 minutes, normal temperature place for 20 minutes, 20 minutes of reper-fusion.The solution of the cardiac muscle tissue of the rats were treated with saline and then the accounts of malondialde -hyde (MDA)and the activity of superoxide dismutase (SOD) , and the changes of left ventricular end-diastolic pressure ( LVEDP) were determined to compare the different protective effects .Results The accounts of MDA in the control group were the highest , there was a significant difference between the experimental group and the controls concerning with the re -sults of ischemia period and reperfusion period (P<0.01, P<0.05).There were differences among the ischemia period and reperfusion period and preischemia period in the control group (P<0.05).In the experimental group, there was not significant difference among the ischemia period and reperfusion period and the preischemia period .There was a significant difference between the experimental group and the controls considering the activity of SOD (P<0.01).The accounts of LVEDP of the control group was obviously high (P<0.05).The level of LVEDP in experimental group was obviously lower than in the control group (P<0.05),but had no significant difference to ischemia period .Conclusion Hydrogen rich sa-line is quite effective in alleviating myocardial ischemia reperfusion injury .%目的：探讨氢气对心肌缺血再灌注（ I／R ）损伤的保护作用。方法将48只大鼠随机分为实验组和对照组各24只。取两组大鼠心脏，按逆灌注10 min，常温旷置20 min、再灌注20 min的方法建立心肌缺血再灌注模型。对照组灌注液用K-R液，实验组灌注液用K-R液＋氢气饱和生理盐水。监测两组大鼠心脏缺血前期、缺血期、再灌注期心肌组织丙二醛（MDA）、超氧化物歧化酶（SOD）水平及左室舒张末期压力（LVEDP）。结果对照组缺血期心肌MDA水平高于缺血前期（P＜0．05），再灌注期心肌MDA水平低于缺血期（P＜0．05），但仍高于缺血前期（P＜0．05）。实验组各期心肌MDA水平无统计学差异；缺血期、再灌注期心肌MDA水平较对照组同期下降（P均＜0．05）。两组缺血期与缺血前期心肌SOD水平无统计学差异，缺血再灌注期心肌SOD水平低于缺血前期和缺血期（P均＜0．05）。实验组缺血期与再灌注期心肌SOD水平较对照组同期升高（P均＜0．05）。对照组再灌注期LVEDP高于缺血前期（P＜0．05）；实验组再灌注期与缺血前期LVEDP无统计学差异，但与对照组同期比较下降明显（P＜0．05）。结论氢气对大鼠离体心脏心肌I／R损伤有明显的保护作用。其机制可能为抑制心肌组织MDA表达，提高心肌组织SOD水平。