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目的 :探讨非创伤性下肢缺血预处理对大鼠心肌保护效应的机制。方法 :用雄性SD大鼠 36只 ,分对照、缺血再灌注、经典缺血预处理及非创伤性下肢缺血预处理 4组。分别观察以下指标 :血浆一氧化氮 (NO)水平 ;心肌热休克蛋白 70 (HSP70 )mRNA表达 ;心肌 5’ -核苷酸酶 (5’ -NT)及过氧化氢酶 (CAT)活性。结果 :经典及非创伤性下肢缺血预处理后 ,血浆NO水平显著高于缺血再灌注组和对照组 (P <0 0 1) ,心肌HSP 70mRNA表达明显增强 ,心肌 5’ -NT、CAT活性升高 (P <0 0 5 ,vsI/R) ,而经典及非创伤性下肢缺血预处理两组间上述指标无显著差异 (P >0 0 5 )。结论 :非创伤性下肢缺血预处理保护心肌的机制可能与经典缺血预处理相似 ,均是通过提高心肌内源性保护物质NO、HSP70mRNA、CAT及 5’ -NT显示预处理效应。
Objective: To explore the mechanism of non-traumatic ischemic preconditioning on myocardial protective effect in rats. Methods: Thirty-six male Sprague-Dawley rats were randomly divided into four groups: control, ischemia-reperfusion, classic ischemic preconditioning and non-traumatic lower limb ischemia. The following indexes were observed: the level of plasma nitric oxide (NO); the expression of heat shock protein 70 (HSP70) mRNA; the activity of 5’-nucleotidase (5’-NT) and catalase (CAT) Results: Plasma NO levels were significantly higher in ischemic preconditioning and non-traumatic lower extremities than those in ischemia-reperfusion group and control group (P <0.01). The expression of HSP70 mRNA in myocardium was significantly increased. The myocardial 5 ’-NT, CAT (P <0.05, vsI / R), while there was no significant difference between the two groups in the classic and non-traumatic ischemic preconditioning (P> 0.05). CONCLUSION: The mechanism of non-traumatic ischemic preconditioning to protect myocardium may be similar to that of classical ischemic preconditioning, both of which are through the enhancement of myocardial endogenous protective substances NO, HSP70mRNA, CAT and 5 ’-NT.