背景:近几年来,大量研究发现低浓度氢气或富氢水或氢气饱和生理盐水对多种疾病具有神奇的保护作用,包括心肌缺血再灌注损伤.目的:探讨富氢水对心肌缺血再灌注损伤的保护作用.方法:将48只Wistar大鼠随机分为对照组与富氢水组,2组再分别随机分成缺血前期、缺血期、缺血再灌注期,每期8只大鼠.取大鼠心脏,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.对照组采用预先用氧平衡(体积分数95%O2+5%CO2)的37 ℃ K-R 液灌注,富氢水组采用预先用氧平衡(体积分数95%O2+5%CO2)的37 ℃ K-R液+富氢水灌注(0.6 mmol/L,pH 7.3).实验完毕后取材,苏木精-伊红染色观察两组大鼠心肌组织的心肌病理学改变,测定心肌组织中乳酸脱氢酶、肌酸激酶的活性,双抗夹心ELISA法检测肿瘤坏死因子α、白细胞介素1β的水平.结果与结论:①对照组缺血期与缺血再灌注期心肌乳酸脱氢酶活性均高于缺血前期(P < 0.05);富氢水组各期心肌乳酸脱氢酶活性差异无显著性意义;与对照组相比富氢水组缺血再灌注期乳酸脱氢酶活性明显降低(P < 0.05);②对照组缺血再灌注期肌酸激酶活性均显著高于缺血前期和缺血期(P < 0.05);富氢水组各期肌酸激酶活性差异无显著性意义;与对照组比较富氢水组缺血再灌注期肌酸激酶活性明显降低(P < 0.05);③对照组和富氢水组缺血再灌注期肿瘤坏死因子α、白细胞介素1β均显著高于缺血期和缺血前期(P < 0.05);缺血期高于缺血前期(P < 0.05);与对照组相比富氢水组缺血再灌注期两因子水平明显降低(P < 0.05),但仍高于缺血前期;④结果说明,富氢水对离体大鼠心脏心肌缺血再灌注损伤有保护作用,其机制可能是降低肿瘤坏死因子α、白细胞介素1β水平的表达,即减少了炎症反应.%BACKGROUND: Increasing evidence has indicated that low-concentration hydrogen or hydrogen rich water or hydrogen saturated saline exerts a protective effect on various diseases, such as myocardial ischemia/reperfusion injury. OBJECTIVE: To explore the protective effect of hydrogen rich water on myocardial ischemia/reperfusion injury. METHODS: Forty-eight Wistar rats were equally randomized into control and hydrogen-rich groups, and then subdivided into ischemic preconditioning, ischemia, and ischemia/reperfusion groups (n=8 rats in each subgroup). The myocardial ischemia/reperfusion model was established in the heart of each rat by the following procedures: reverse perfusion for 10 minutes, room temperature for 20 minutes, and reperfusion for 20 minutes. The control rats was perfused with pre-oxygenated (95% O2plus 5% CO2) 37 ℃ K-R solution and the hydrogen-rich group was perfused with pre-oxygen-equilibrated (95% O2plus 5% CO2) 37 ℃ K-R solution plus hydrogen-rich water (0.6 mmol/L, pH=7.3). Subsequently, the heart was removed, the pathological changes of the myocardial tissues were observe by hematoxylin-eosin staining, the activities of lactic dehydrogenase and creatine kinase in the myocardial tissues were determined, and the levels of tumor necrosis factor-α and interleukin-1β were detected by ELISA. RESULTS AND CONCLUSION: In the control group, the activity of lactic dehydrogenase at the ischemic and ischemia/reperfusion stages was significantly higher than that at the ischemic preconditioning stage (P < 0.05), and the activity of creatine kinase at the ischemia/reperfusion stage was significantly higher than that at the ischemic preconditioning and ischemic stages (P < 0.05). In the hydrogen-rich group, there was no significant difference in the activities of lactic dehydrodenase and creatine kinase at each stage, but the activities of at the ischemia/reperfusion stage was significantly lower than those in the control group (P < 0.05). In the two groups, the order of the levels of tumor necrosis factor-α and interleukin-1β was as follows: the ischemia/reperfusion stage > ischemic stage > ischemic preconditioning stage (P < 0.05). The levels of above factors in the hydrogen-rich group were significantly lower than those in the control group (P < 0.05). Our findings imply that hydrogen rich water has protective effect on myocardial ischemia/reperfusion injury of the rat hearts in vitro,which may be by reducing the expression of tumor necrosis factor-α and interleukin-1β, and further alleviating the inflammatory response.
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