摘要
目的 判断全身亚低温治疗的心脏效应及其临床使用的安全性。方法 5 8只Wistar大鼠随机分成假手术组 (Ⅰ组 ,n =10 )、脑梗死常温组 (Ⅱ组 ,n =2 4 )和脑梗死亚低温组 (Ⅲ组 ,n =2 4 ) ,采用线栓法制作大脑中动脉 (MCA)梗死模型。测定术后 12h的心肌高能磷酸化合物 (ATP、ADP和AMP)及能量储备(EC)值 ,动态监测梗死组的异常ECG发生率 ,观察心肌的超微结构改变。结果 缺血后 12h时Ⅱ和Ⅲ组鼠心肌的ATP、ADP及EC均较Ⅰ组下降 (P <0 .0 1) ,但Ⅲ组ATP及EC较Ⅱ组增高 (P <0 .0 1) ;缺血后Ⅲ组鼠心率 (HR)较Ⅱ组明显降低 (P <0 .0 1) ,Ⅲ组异常ECG发生率与Ⅱ组比较无明显差异 ;超微结构显示Ⅱ和Ⅲ组结构均较Ⅰ组差 ,但Ⅲ组优于Ⅱ组。结论 全身亚低温治疗在一定程度上改善了因应激性缺血而下降的心肌能量储备及缺血对心肌超微结构的影响 ,且不产生严重的心电生理异常 ,其临床使用是安全的。
Objective To determine effects of the therapeutic systemic hypothermia on heart and its safety. Methods 58 Wistar rats were divided into sham operated group (group Ⅰ n =10), normothermia infarction group (group Ⅱ n =24) and mild hypotheamia infarction group (group Ⅲ n =24) at random. The animal model of reformed milddle cerebral artery occlusion (MCAO) was made. In infartion group the myocardial high energy phosphale (ATP, ADP, AMP) and energy charge (EC) were detcted in 12 hours after ischemia. The abnormal electrocardiograph (ECG) and myocardial ultrastructure was observed. Results The ATP, ADP and EC in group Ⅱ, Ⅲ were lower than those of group Ⅰ in 12 hours after ischemia ( P < 0.01 ), but ATP, EC in group Ⅲ is higher than group Ⅱ ( P < 0.01 ); The heart rate (HR) after ischemia in group Ⅲ was lower than group Ⅱ ( P < 0.01 ); The rate of abnormal ECG between group Ⅲ and group Ⅱ wasn't significantly different; Myocardial ultrastructure of group Ⅲ was better than that of group Ⅱ. Conclusion The systemic mild hypothermia therapy may ameliorated myocardial EC due to stressed ischemia and the changes of ischemic myocardial ultrastructure, It is safe and doesn't cause severe abnormality of cardiac electrophysiology.
出处
《卒中与神经疾病》
2002年第3期134-137,共4页
Stroke and Nervous Diseases
关键词
亚低温
治疗
大鼠
局灶性脑缺血
心脏
心电生理
心肌超微结构
Mild hypothermia Focal brain ischemia Myocardial high energy phosphate Cardiac electrophysiology Myocardial ultrastructure