Ca^(2+)预处理和缺血预处理对大鼠心脏Ca^(2+)反常损伤的影响

The effect of Ca^(2+) preconditioning and ischemic preconditioning on Ca^(2+) paradox injury in rat Heart

给离体大鼠心脏进行5次1分钟无Ca^(2+)继5分钟复Ca^(2-)灌流预处理后,可使随后Ca^(2-)反常损伤明显减轻,表现为心肌细胞蛋白质丢失量减少,冠状动脉痉挛减轻.本研究进一步应用2次10分钟缺血,继10分钟再灌注进行缺血预处理,结果显示这一方案未能减轻Ca^(2+)反常所致心肌损伤.如在Ca^(2-)预处理过程中给予腺苷A_1受体阻滞剂8-SPT,可以阻断Ca^(2+)预处理的保护作用,提示腺苷A_1受体兴奋可能是这一保护机制的重要环节.

Repeated calcium depletion and repletion of short term duration Ca2+ preconditioning CPC is hypothesized to protect the heart from lethal injury after exposing it to the Ca2+ paradox (Ca2+ PD). Hearts were preconditioned with five cycles of Ca2+ depletion (1 minute) and Ca2+ repletion (5 minutes). These hearts were then subjected to Ca2+ PD,ie,one cycle of Ca2+ depletion (ten minutes) and Ca2+ repletion (ten minutes). Hearts subjected to the Ca2+ PD underwent rapid and severely injury. CPC showed remarkable protection against the Ca2+ PD injury. Protein release from the perfusated heart was significantly reduced in CPC hearts compared with nopreconditioned Ca2+ PD hearts (0. 56 + 0. 10 and 1. 23 + 0. 10 mg/ml respectively ,P<0. 01). Coronary flow of CPC hearts was greater than Ca2+ PD hearts (3. 4 + 0. 3 and 2. 5 + 0. 6 ml/min respectively ,P<0. 05). Addition of the adenosine A1 receptor antagnist 8- (P-sulgophenyl)-theophylline before and during CPC blocked the benifcial effects of CPC. The study futher observed that an ischemic preconditioning protocal, two cycles of ten minute ischemia and ten minute reperfusion. did not exert protction against Ca2+ PD injury. The present study suggests that Ca2+ preconditioning confer significant protection against the lethal injury of Ca2+ PD in rat heart. Adenosine A1 recepter appears to be involved in this protection mechanisms.