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作 者:夏照帆[1] 宋智钢[1] 徐志云[1] 张宝仁[1]
机构地区:[1]第二军医大学长海医院
出 处:《第二军医大学学报》1999年第1期9-13,共5页Academic Journal of Second Military Medical University
基 金:国家自然科学基金;国家杰出青年科学基金;上海市卫生系统百名跨世纪优秀学科带头人培养计划资助项目
摘 要:目的:观察不同心肌保护方法对缺血心肌细胞内能量代谢及离子平衡的影响,探讨冷停搏液对缺血心肌的保护机制。方法:用Langendorf技术对离体大鼠心脏进行灌注,灌注液采用改良Krebs-Henseleit溶液,含3.5mmol/LTm(DOTP)5-(钠位移剂)。实验分4组:Ⅰ组37℃条件下缺血60min,再灌注30min;Ⅱ,Ⅲ组分别给予缺血前高钾停搏液灌注5min或缺血期低温保护(15℃);Ⅳ组给予缺血前高钾停搏液灌注和缺血期低温保护,再灌注时间和条件各组均相同。缺血及复灌期间采用31P-NMR和23Na-NMR谱持续检测心肌细胞内ATP,Pcr,Phi,Nai及Pi的变化,同时通过放置于左室内的气囊记录左室功能。结果:Ⅰ组缺血后15minATP,Pcr波谱信号无法测出,出现严重细胞内酸中毒及钠潴留。Ⅱ组在缺血后15minATP,Pcr分别为(11.1±1.9)和(2.6±1.3)μmol/g,缺血后30min出现与Ⅰ组相似的变化,但钠潴留较Ⅰ组减轻。Ⅲ组ATP,Pcr,Phi,Nai的变化较Ⅰ,Ⅱ组明显减轻。Ⅳ组缺血期ATP及Nai无明显变化。Ⅲ,Ⅳ组复灌后左心功能可恢复正常。结论:低温对缺血心肌代谢和?Objective: To assess the protective mechanism of cold cardioplegia in ischemic hearts by observating effects of different protective methods on ischemic myocardial intracellular energy metabolism and ion homeostasis. Methods: Isolated rat hearts were perfused in a Langendorff preparation with a modified Krebs Henseleit medium with 3.5 mmol/L Tm(DOTP) 5- , a sodium shift agent. Experimental groups underwent 60 min ischemia(groupⅠ) either after a 5 min perfusion of hyperkalemic cardioplegia(groupⅡ) or at 15℃(group Ⅲ), or with both interventions(group Ⅳ), followed by 30 min of reperfusion. Interleaved 31 P and 23 Na NMR spectra were continuously monitored to measure ATP, Pcr,Ph i,Na i and P i during ischemia and reperfusion. Left ventricular function was monitored with an intraventricular balloon simultaneously. Results: The myocardium showed intracellular acidosis and sodium accumulation severely in group Ⅰ, ATP and Pcr of which being not detected after 15 min of ischemia. After 30 min of ischemia, the changes of group Ⅱ were similar to those of group Ⅰ. The changes of group Ⅲ were more slight compared to groupⅠ and Ⅱ during ischemia. ATP and Na i of group Ⅳ were maintained. The left ventricular function was preserved in group Ⅲ and Ⅳ after reperfusion. Conclusion: Hypothermia as the sole intervention was more effective than hyperkalemic on ischemic myocardial metabolism and function. The combination of hypothermia and hyperkalemia could prevent ischemic myocardium from intracellular acidosis and eliminate sodium accumulation effectively, so it plays a greater protective role in ischemic myocardial function.
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