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作 者:赵振林[1] 李家成[1] 王敬弘[2] 马杰[1] 郭光伟[1]
机构地区:[1]山西医科大学第二附属医院心胸外科,太原030001 [2]长治医学院附属医院心胸外科
出 处:《中华实验外科杂志》1999年第6期543-544,共2页Chinese Journal of Experimental Surgery
基 金:山西省科委资助项目
摘 要:目的 探讨T3 增补于停搏液中的心肌保护作用。方法 离体鼠心( n = 16) 在改良的LangendorffNeely 灌注模型上、37 ℃下经历20 分钟预灌注、20 分钟停搏、30 分钟再灌注。结果 再灌注30 分钟时,左室功能指标(LVDPdp/dt)百分恢复率治疗组显著高于对照组( P <0 .01),心肌超氧化物歧化酶(SOD) 治疗组显著高于对照组( P< 0.01),过氧化脂质(LPO) 治疗组显著低于对照组( P <0.05);心肌酶(HBDH.LDH)释放量再灌注期对应时点组间比较,治疗组显著低于对照组( P< 0 .01) ;电镜观察心肌超微结构,治疗组显著优于对照组。结论 T3 增补于心脏停搏液中可以显著地促进缺血后左室功能的恢复,显著减轻心肌缺血再灌注损伤,具有良好的心肌保护作用。Objective To study the protective effects of triiodothyronine supplement in cardioplegia on postischemic myocardium. Methods Isolated rat hearts (n=16) were subjected to preperfusion for 20 min, ischemia for 20min and reperfusion for 30 min using a modified Langendorff Neely model with modified Krebs Henseleit buffer at 37℃. Results Percent recovery of left ventricular developing pressure (LVDP) and its first derivate (dp/dt) in the treated group 30 min after reperfusion were significantly increased as compared with control group (P<0.01). Comparison of postischemic myocardial superoxidas dismutase (SOD) between two groups demonstrated a significant increase in the treated group (P<0.01), while the comparison of postischemic myocardial lipid peroxide (LPO) between two groups demonstrated a significant decrease in the treated group (P<0.05). The release of postischemic myocardial enzyme (HBDH, LDH) in the treated group was significantly lower than in the control group (P<0.01). Myocardial ultrastructure was well preserved in the treated group. Conclusion T 3 supplement in cardioplegia significantly improve the recovery of postischemic left ventricular function, alleviated reperfusion mediated myocardial injury after global ischemia, suggesting good myocardioprotective actions.
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