浅低温对急性心肌梗死保护作用的研究进展 |
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引用本文: | 阮爱兵[综述] 吕爱玲[综述] 方五旺[审校]. 浅低温对急性心肌梗死保护作用的研究进展[J]. 医学综述, 2013, 0(24): 4479-4481 |
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作者姓名: | 阮爱兵[综述] 吕爱玲[综述] 方五旺[审校] |
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作者单位: | 芜湖市第二人民医院心内科,安徽芜湖241000 |
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摘 要: | 许多动物实验研究表明,急性心肌梗死后浅低温(32~34℃)是一种有效的干预手段,能够降低梗死面积,改善梗死心肌的愈合。但要使治疗性低温产生保护效应必须在心肌缺血发生后尽可能早地而且在再灌注之前就要使心肌达到目标温度。对心肌产生保护作用的浅低温对左心室功能、局部心肌血流及缺血预适应似乎不会产生损害作用。浅低温保护作用的机制还未完全阐明,可能包括降低组织代谢率,保存高能磷酸盐,减轻细胞凋亡,诱导热休克蛋白的产生等。
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关 键 词: | 浅低温 急性心肌梗死 心肌保护 |
Protective Effect of Mild Hypothermia on Acute Myocardial Infarction |
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Affiliation: | RUAN Ai-bing;LV Ai-ling;FANG Wu-wang;Department of Cardiology,Wuhu Second People's Hospital; |
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Abstract: | In many animal models,mild therapeutic hypothermia( 32-34 ℃) is a powerful intervention, reducing myocardial infarct size and improving healing after infarction. It has been shown in experimental and clinical studies that for therapeutic hypothermia to be effective it must be initiated as early as possible after the onset of ischemia before reperfusion. The reduction in temperature necessary to produce cardioprotection appears to have no detrimental effects on left ventricular function or regional myocardial blood flow and ischemic preconditioning. The mecnhanisms of protection produced by hypothermia have yet to be conclusively determined but may include a decrease in tissue metabolic rate,preservation of high energy phosphates,a reduction in tissue apoptosis or induction of heat shock proteins. |
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Keywords: | Mild hypothermia Acute myocardial infarction Cardioprotection |
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