鹿茸精的心肌保护作用机理  

Mechanism of Pantocrium Anti-reperfusion Injury

作　　者：屈立新[1] 唐越[2] 王向东[1] 敖定椿[2] 郭遂群[1] 

机构地区：[1]第一军医大学南方医院胸心外科,广州510515 [2]大连医科大学心血管病研究所

出　　处：《中华实验外科杂志》1999年第1期66-67,共2页Chinese Journal of Experimental Surgery

摘　　要：目的探讨鹿茸精常温下抗心肌缺血再灌注损伤的作用机制。方法应用体外循环动物心脏模型进行研究，将犬随机分成二组。Ⅰ组：主动脉阻断前静脉输入鹿茸精（50mg／kg）；Ⅱ组：主动脉阻断前静脉输入异搏定（0.1mg／kg）。结果再灌注60分钟与再灌注30分钟相比，异搏定显著降低心肌收缩功能（LVSP，＋dP／dtmax；P＜0.01，P＜0.05）。鹿茸精组Ca^（++）－mg（++）－ATPase活性显著高于异搏定组（P＜0.01）。而细胞内游离钙显著低于异搏定组（P＜0.01）。结论鹿茸精抗再灌注损伤的机制是防止钙超负荷，加强心肌ATP合成，保护心肌细胞膜完整性并促进心肌功能恢复。Objective To investigate the mechanism of Pantocrinum protecting myocardium from reperfusion injury after normothermic ischemia. Method Sixteen dogs were randomly divided into two groups: group Ⅰ (n = 8) received intravenous Pantocrinum (50 mg/kg) before aortic cross-clamping, while group Ⅱ (n = 8) was given intravenously verapamil (0.1 mg/kg) before aortic cross-clamping. Result Verapamil reduced global contractility significantly after 30 min and 60 min after reperfusoin as compared with group Ⅰ (LVSP and + dp/dt max: P < 0.01, P < 0. 05). Ca（2+） -Mg（2+） -ATPase activities in Group Ⅰ were higher than in group Ⅱ（P < 0. 05）, on the contrary, intracellular free calcium concentration is much lower than in group Ⅱ Conclusion The mechanism of Pantocrinum anti-reperfusion injury is to prevent intracellular calcium from overloading, enhance the synthesis of ATP, preserve the integrity of myocardial cell membrane and improve the recovery of myocardial function.

关 键 词：鹿茸精 心肌保护 再灌注损伤 动物模型 

分 类 号：R542.2[医药卫生—心血管疾病] R965[医药卫生—内科学]