去甲肾上腺素预处理对大鼠供心超氧化物歧化酶及丙二醛表达的影响

目的探讨去甲肾上腺素预处理对大鼠供心心肌细胞超氧化物歧化酶(SOD)及丙二醛(MDA)表达的影响。方法雄性Wistar大鼠18只随机分为对照组和实验组各9只,对照组腹腔注射生理盐水0.5 mL,24 h后取离体心脏灌注Histidine-tryptophan-ketoglutarate心脏保护液,4℃保存3 h后建立Langendorff离体心脏灌注模型,灌注Krebs-Henseleit液2 h;实验组腹腔注射重酒石酸去甲肾上腺素(溶于生理盐水)3.1μmol.kg-1(0.53 mg.kg-1),24 h后取离体心脏,处理方法同对照组。测定2组肌酸激酶(CK)、乳酸脱氢酶(LDH)漏出率以及心肌水含量(MWC)、SOD、MDA的水平。结果实验组SOD的水平较对照组明显升高(P<0.01);MWC、MDA含量、CK、LDH漏出率较对照组明显降低(P<0.01)。结论去甲肾上腺素预处理能促进SOD表达,降低MDA含量,对抗氧自由基损伤,从而发挥对离体大鼠供心心肌的保护效应。

Effects of norepinephrine preconditioning on expressions of superoxide dismutase and malondialdehyde in myocardial cell of isolated rat's heart

Objective To investigate the effects of norepinephrine preconditioning on expressions of superoxide dismutase（SOD） and malondialdehyde（MDA） in myocardial cell of isolated rat′s heart.Methods Eighteen male Wistar rats were randomly divided into control group and experimental group,nine rats in each group.The control group was injected intraperitoneally saline solution 0.5 mL and 24 hours later the isolated hearts were stored in 4 ℃ for 3 hours with histidine-tryptophan-ketoglutarate（HTK） solutions,and then isolated hearts were perfused for 2 hours by Krebs-Henseleit to establish the Langendorff model.Experimental group was injected intraperitoneally noradrenaline bitartrate 3.1 μmol·kg-1（0.53 mg·kg-1） and 24 hours later isolated hearts were stored in 4 ℃ for 3 hours with HTK,and then isolated hearts were perfused for 2 hours by Krebs-Henseleit to establish the Langendorff model.Myocardial SOD,MDA content,myocardial water content（MWC）,lactate dehydrogenase（LDH） and creatinekinase（CK） leakage rate were detected.Results SOD content in the experimental group was significantly higher than that in control group（P0.01）;MWC,MDA content and CK,LDH leakage rate were significantly lower than those in control group（P0.01）.Conclusion This study demonstrates that norepinephrine preconditioning can promote the expression of SOD and reduce the MDA content in isolated rat hearts,and play the role of anti-oxidation to protect myocardial cells against ischemia-reperfusion injury.