不同温度下缺血预处理对离体大鼠心脏缺血-再灌注损伤的心肌保护

Protective effects of ischemic preconditioning with normothermia or hypothermia on schemia/reperfusion in-jury in isolated rat hearts

观察离体大鼠Langendroff灌注心脏模型,37℃和30℃条件下,单次5min缺血、10min再灌注所形成的缺血预处理,对持续180min缺血、45min再灌注的心肌的保护作用.持续缺血期间控制心脏局部温度在20℃左右,并间隔30min经主动脉根部灌注St.Thomas晶体心麻痹液.实验发现,常温条件下,5min短暂缺血并不能引起大鼠心肌顿抑.常温下缺血预处理与晶体心麻痹液相结合,对离体大鼠灌注心脏缺血再灌注损伤的保护作用呈累加现象;低温下缺血预处理使预处理的心肌保护作用减弱,可能与心脏停跳前的快速降温有关;心肌顿抑不是预处理的可能机制;能量需求减少和细胞结构的保护可能是预处理的机制之一.

Using isolated rat hearts perfused on a langendorff apparatus,ischemic preconditioning (IP) was investigated with 5 min normothermic (at 37℃) or hypothermic (at 30 ℃) ischemia, followed by 10 min of reperfusion before the arrest period, as an adjunct to St. Thomas crystalloid cardioplegia during 180 min ischemia. After basline functional data were obtained, IP was induced 1 control hearts underwent no IP. Results showed that IP improved functional recovery from ischemia during 45 min reperfusion in normothermic ischemic preconditioning group (NP) comparing with normothermic control (NC),P<0. 01 ,and that IP reduced leakage of enzymes (CK,LDH,GOT). We also detected that the content of adenosine triphosphate (ATP) in myocardium was higher in NP than in NC,34- 29± 4. 13μmol/g vs 10. 45±5. 09 μmol/g (P<0. 01). Ultrastrustructural observation showed that irreversible injury was homogeneuos in control but only mild and local in NP. Hypothermic ischemic preconditioning brought about a significant preservation in release of enzymes (P<0. 01). These data indicate that NP can improve recovery of cardiac function and may be additive with crystalloid cardioplegia after global ischemia 180min in isolated rat heart,and that hypothermic ischemic preconditioning can decrease the protective effects, perhaps related to the adverse effect of prearrest cardiac hypothermia. We consider that my-ocardial stunning may not be the mechanism of IP, and eigher preservation of ATP or delaying ischemic cell death may be responsible for the preconditioning.