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目的:探讨褪黑素对脓毒症心肌损伤的作用及其机制。方法:30只SPF级雄性SD大鼠随机分为正常对照组、脓毒症组、褪黑素预处理组。采用盲肠结扎穿刺法制作脓毒症大鼠模型,褪黑素预处理组术前7d每日腹腔注射褪黑素4mg/kg。盲肠结扎穿刺术后12h经右颈总动脉左心室内插管监测各组大鼠LVSP、LVEDP、±dp/dt max等血流动力学指标,收集大鼠血清检测肌酸激酶同工酶CK-MB、乳酸脱氢酶LDH的含量,测定大鼠心肌组织MDA、SOD和tNO含量。结果:脓毒症组大鼠LVSP、±dp/dt max均有所降低,LVEDP升高,而褪黑素预处理组以上各项指标均有不同程度改善;脓毒症模型组大鼠血清CK-MB、LDH以及心肌组织MDA、NO含量均明显升高,心肌组织SOD含量明显减少(P<0.05);褪黑素预处理明显降低了大鼠血清CK-MB、LDH以及心肌组织MDA、NO含量,增加了大鼠心肌组织SOD的活力。结论:褪黑素预处理通过抑制氧化损伤,减轻脓毒症心肌损伤。
Objective: To investigate the effect of melatonin on myocardial injury induced by sepsis and its mechanism. Methods: Thirty SPF male SD rats were randomly divided into normal control group, sepsis group and melatonin preconditioning group. The model of sepsis was made by cecal ligation and puncture. Melatonin pretreatment group was intraperitoneally injected with 4 mg / kg of melatonin 7 days before operation. After 12 hours of cecal ligation and puncturing, the left hemodynamic parameters of LVSP, LVEDP and ± dp / dt max were detected by left ventricular catheterization of the right common carotid artery. Serum levels of creatine kinase CK- MB, lactate dehydrogenase LDH content, determination of myocardial tissue MDA, SOD and tNO content. Results: The levels of LVSP and ± dp / dt max in the sepsis group decreased and the LVEDP increased, while those in the melatonin pretreatment group all improved to some extent. In the sepsis model group, serum CK (P <0.05). Pretreatment with melatonin significantly reduced serum levels of CK-MB, LDH, and myocardial MDA, NO, -MB and LDH, as well as myocardial MDA and NO levels Content, increased the activity of SOD in myocardial tissue of rats. Conclusion: Melatonin preconditioning can relieve the myocardial injury of sepsis by inhibiting oxidative damage.