亚低温治疗对实验性脑梗死大鼠心脏功能的影响

背景实施亚低温可能对全身各重要脏器的功能和代谢产生一定影响,这些影响有利还是有弊,需要进一步研究考证.目的在亚低温治疗脑梗死的同时测定心脏的能量储备,心电图,观察其超微结构,从而探讨亚低温对心脏功能的影响.设计随机对照实验.单位武汉大学人民医院神经内科.材料实验在武汉大学人民医院神经内科实验室完成.选择SD大鼠58只,随机分为假手术组10只,脑梗死后常温组(简称常温组)24只,脑梗死后亚低温治疗组(简称亚低温组)24只.方法常温组、亚低温组采用线栓法制作大脑中动脉梗死模型,假手术组仅切开皮肤及结扎血管,不穿线入大脑中动脉.亚低温组动物置于4℃环境中将动物肛温控制在(34±1.0)℃;假手术组、常温组动物置于室温(20℃)环境中.12 h后测定心肌组织的三磷酸腺苷、二磷酸腺苷和磷酸腺苷值及能量储备值,并于电镜下观察心肌超微结构改变.主要观察指标①各组大鼠心肌能量代谢的改变.②各组大鼠心电生理改变.③各组大鼠心肌超微结构.结果58大鼠均进入结果分析.①缺血后12 h时常温组和亚低温组大鼠心肌三磷酸腺苷、二磷酸腺苷、能量储备值均低于假手术组(P＜0.01),但亚低温组的三磷酸腺苷和能量储备值却高于常温组(P＜0.01).②常温组和亚低温组异常心电图发生率差异无显著性意义(P＞0.05);但亚低温组的心率明显低于常温组[(290.92±44.18),(472.20±12.79)次/min,P＜0.01],有3只大鼠的心率低于150次/min.③超微结构显示常温组和亚低温组心肌均有缺血性损伤,但亚低温组的损伤较常温组轻.结论全身亚低温治疗脑梗死时可显著减缓心率,改善心肌的能量储备,减轻脑梗死引起的心肌缺血,不会增加心电图异常的发生率.

Effect of mild hypothermia on cardiac function in rats with experimental cerebral infarction

BACKGROUND: Mild hypothermia might in some degree affect the functions and metabolism of the vital organs, and its effects can be harmful sometimes but may also be favorable on some other occasions, which remained to be further studied.OBJECTIVE: To examine the effect of mild hypotherrnia on cardiac function of rats with experimental cerebral infarction by observing the changes in the cardiac energy reserve and electrocardiogram (ECG) manifestations,as well as the ultrastructural changes of the myocardium.DESIGN: Randomized controlled experiment.SETTING: Department of Neurology, Renmin Hospital of Wuhan University.MATERIALS: This experiment was carried out in the Laboratory of Department of Neurology, Renmin Hospital of Wuhan University. Totally 58SD rats were randomized into sham operation group (n=10), cerebral infarction with normal temperature group (normal temperature group, n=24),cerebral infarction with mild hypothermia treatment group (mild hypothermia group, n=24).METHODS: Middle cerebral artery occlusion (MCAO) was induced in normal temperature group and mild hypothermia group with a suture intro duced into the middle cerebral artery of the rats. The rats in- sham opera tion group were only subjected to skin incision and vessel ligation without suture insertion into the middle cerebral artery. The rats in mild hypother mia group were kept at 4 ℃ with their anal temperature maintained at (34±1.0) ℃, while the rats in sham operation group and normal tempera ture group w ere kept at room temperature (20 ℃). Twelve hours later, the levels of myocardial ATP, DTP, adenosine phosphate and energy reserve were determined, and the changes in myocardial ultrastructure were ob served under electron microscope. MAIN OUTCOME MEASURES: ① Changes of myocardial energy metabolism; ② Changes of cardiac electrophysiology; ③ Ultrastructural changes of the myocardium. RESULTS: All the 58 rats survived the operation and all enter the re sult analysis. The levels of myocardial ATP, DTP and energy reserve were significantly lowered in normal temperature group and mild hypothermia 12 hours after the ischemia in comparison with the sham operation group (P ＜ 0.01), but the level of ATP and energy reserve in mild hypothermia group was higher than those of normal temperature group (P ＜ 0.01). No significant difference was noted in ECG abnormality rate between normal temperature group and mild hypothermia group (P ＞ 0.05), but the heart rate was found obviously lower in mild hypothermia group [(290.92±44.18) vs (472.20±12.79) bpm, P ＜ 0.01], with 3 rats showing heart rate less than 150 bpm. Ultrastructural observation revealed the presence of my ocardial ischemic impairment in normal temperature group and mild hy pothermia group, but the impairment in mild hypothermia group was less severe. CONCLUSION: Heart rate can be markedly reduced during general mild hypothermia treatment for cerebral infarction to improve myocardial energy reserve and alleviate myocardial ischemia due to cerebral infarction without increasing the abnormality rate of ECG.