摘要
目的：体外反搏在治疗许多缺血性疾病中有良好的效果，本文在重症失血性休克模型上探讨其保护机制。方法：采用一侧颈总动脉插管放血制造重症失血性休克模型，全程监测血压，实验结束时取左室心肌进行各项检查。结果：①反搏组反搏后血压显著高于反搏前，且实验结束时反搏组的血压也显著高于失血组。②失血组心肌内ＡＴＰ水平显著低于对照组及反搏组，而乳酸含量显著高于对照组及反搏组。③失血组心肌ＭＤＡ含量显著高于对照组及反搏组，而ＳＯＤ的活性则显著低于反搏组及对照组。
Abstract AIM:To explore the protective mechanisms of ECP (external counterpulsation) on ischemia diseases such as coronary heart disease, ischemia apoplexy and hemorrhagic shock (HS). METHODS:The model of serious hemorrhagic shock was used. After the whole experiment , hearts were excised to detect parameters of energy and free radical metabolism. RESULTS:Blood pressure of ECP and C groups at the end of experiment was significantly higher than that of HS group. ATP level in ventricular tissue of HS group was significantly lower than that of control and ECP groups ( P <0 05), and lactic acid concentration in ventricular tissue of HS group was significantly higher than that of control and ECP groups ( P <0 05), SOD activity of HS group was significantly lower than that of control and ECP groups ( P <0 05), and MDA concentration of HS group was significantly higher than that of control and ECP groups ( P <0 05).CONCLUSION: ECP protected the canine heart of HS and its mechanism may be related to improvement of metabolism of energy and free radical. MeSH Counterpulsation; Energy metabolism; Free radicals; Myocardium
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1998年第6期631-633,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
