氢气对大鼠离体心肌缺血再灌注损伤的保护作用及机制

发布时间：2018-11-01 20:21

【摘要】：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(P0.05),再灌注期心肌MDA水平低于缺血期(P0.05),但仍高于缺血前期(P0.05)。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(P0.05);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(P0.05)。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。
[Abstract]:Objective to investigate the protective effect of hydrogen on myocardial ischemia reperfusion (I / R) injury. Methods 48 rats were randomly divided into experimental group (n = 24) and control group (n = 24). Myocardial ischemia-reperfusion model was established by reverse perfusion for 10 min, at room temperature for 20 min, and reperfusion for 20 min. The control group was perfused with K-R solution, the experimental group with K-R solution hydrogen saturated saline. The levels of malondialdehyde (MDA),) superoxide dismutase (SOD) and left ventricular end-diastolic pressure (LVEDP).) in myocardium of the two groups were monitored in the preischemic, ischemic and reperfusion periods. Results the level of myocardial MDA in the control group was higher than that in the ischemic period (P0.05), and the level of MDA in the reperfusion period was lower than that in the ischemic period (P0.05), but still higher than that in the preischemic period (P0.05). There was no significant difference in myocardial MDA level between the experimental group and the control group, but the level of myocardial MDA in the ischemic and reperfusion period was lower than that in the control group (P < 0. 05). There was no significant difference between the two groups in the level of myocardial SOD during ischemia and pre-ischemia. The level of myocardial SOD in ischemia-reperfusion period was lower than that in preischemic period and ischemic period (P0. 05). The level of myocardial SOD in the experimental group was higher than that in the control group during ischemia and reperfusion (all P 0. 05). The LVEDP of the control group was higher than that of the control group (P0.05), while the LVEDP of the experimental group was not significantly different from that of the control group (P0.05). Conclusion hydrogen has obvious protective effect on myocardial I / R injury in isolated rat heart. The mechanism may be to inhibit the expression of MDA and increase the level of SOD in myocardial tissue.
【作者单位】：河北大学附属医院;河北大学化学院;河北大学生理教研室;
【基金】：河北省2013年医学科学研究重点课题计划项目(20130369)
【分类号】：R965

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