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目的 研究一氧化氮在热应激增强停搏液心脏保护中的作用。方法 采用Lengendorff装置灌注离体心脏。心脏低温 (4℃ )保存 4h后 ,再灌注 40min (37℃ )。实验前 2 4h大鼠进行高温处理 (直肠温度 42℃ ,15min)。记录心率 ,冠脉流量、左室内压以及最大变化速率 ,并测定血浆一氧化氮 (NO)浓度和冠脉流出液中肌酸激酶 (CK)释放量 ,心肌组织肿瘤坏死因子 (TNF α)浓度。结果 热应激能显著增强停搏液的心脏保护作用 ,减少肌酸激酶释放量 ,并升高血浆一氧化氮及心肌组织肿瘤坏死因子α浓度。这些作用能被预先给予亚硝基精氨酸甲酯所取消。结论 一氧化氮参与对大鼠心脏热应激诱导的延迟保护 ,其作用与促进肿瘤坏死因子的产生有关。
Objective To study the role of nitric oxide in cardioprotection induced by heat stress in cardioplegia. Methods Lengendorff apparatus was used to perfuse the isolated heart. After 4 h of hypothermia (4 ℃), reperfusion 40 min (37 ℃). The rats were subjected to high temperature treatment (rectal temperature 42 ℃, 15min) 24 hours before the experiment. The heart rate, coronary flow, left ventricular pressure and maximum rate of change were recorded. The levels of plasma nitric oxide (NO) and the release of creatine kinase (CK) in coronary effluent were measured. The levels of tumor necrosis factor (TNF) . Results Heat stress can significantly enhance cardioprotection of cardioplegia, reduce the release of creatine kinase, and increase the levels of plasma nitric oxide and myocardial TNFα. These effects can be pre-given nitrosyl arginine methyl ester canceled. Conclusion Nitric oxide participates in the delayed protection induced by heat stress in rat heart and its function is related to the promotion of tumor necrosis factor.