摘要
内源性Ｃａ￣（２＋）是ＰＫＣ激活的强力因子，心肌长时间缺血前应用外源性Ｃａ（２＋）能否激活ＰＫＣ而保护心肌呢？在９０ｍｉｎ心肌缺血和１８０ｍｉｎ再灌注前分别给大鼠如下处理：３次短暂心肌缺血；３次ＩＰＣ前静注异搏定；３次ＩＰＣ前静注灯盏花素乙（Ｃｈｅｌｅｒｙｔｈｒｉｎｅ，ＣＨＥ）；静脉注射ＣａＣｌ＿２；灯盏花－ＣａＣｌ＿２，静注ＣａＣＩ＿２前，静脉注射灯盏花素乙。静脉注射Ｃａ￣（２＋）与ＩＰＣ能起到相同的心肌保护作用，二组心肌坏死面积较对照组明显减小上ＰＣ对心肌的保护作用可被异搏定消除；ＣａＣａ￣（２＋）及心肌缺血预处理对心肌的保护作用均可被灯盏花素乙所抑制。静注ＣａＣｌ＿２能激活ＰＫＣ而对鼠心肌起保护作用，临床很有希望在ＰＴＣＡ、心脏移植等术前用静注ＣａＣｌ＿２对心肌进行保护。
Cardiac preconditioning is mediated by protein kinase C (PKC). Although endogenous calcium is a potentstimulus of PKC, it remains unknown whether preischemic administration of exogenous calcium can induce PKC.mediated myocardial protection against ischemia.reperfusion injury. Cacium chloride (CaClz3 was administeredthrough femoral vein at a rate of 1.6umol . ml-1. min.1. Calcium.mediated cardiadaption was then linked to PKCby means of the PKC inhibitor Chelerythrine(CHE. 0.4mg/100g). Results indicated that preischemic CaCl2,adininistration reduced myocardial infarction size as effectivelly as ischemic preconditioning(IPC). Benificialeffects of CaCl2 were eliminated by concurrent PKC inhibitor. These results suggest that CaClz, a safe androutinely administered agent, can induce PKC - mediated cardiac preconditioning. Calcium.induced cardioadapta-tion to ischemia.reperBned ischemic events such as PTCA and electic cardiac operations
出处
《重庆医科大学学报》
CAS
CSCD
1999年第1期10-14,共5页
Journal of Chongqing Medical University
