大鼠心脏低温保存及高钾停跳保护作用的ESR研究

ESR STUDY ON THE ISOLATED RAT HEART PRESERVED AT HYPOTHERMIA AND PROTECTED BY CARDIOPLEGIA

用ESR研究大鼠离体心脏低温长时间缺血后再灌注时产生的自由基,并观察心肌超微结构的变化;对临床心脏直视手术中常用的高钾停跳液的保护作用机理进行了分析。实验结果表明超氧自由基信号强度随缺血温度的降低而明显减弱。高钾停跳液保护的大鼠离体心脏于低温(4℃)缺血后再灌15s,4h内超氧自由基信号强度变化不明显。缺血4h后再灌注,实验组心脏全部于15s内自动复跳,超微结构的变化轻微。以上改变与对照组比较有明显的差异。本实验为低温保存心脏及高钾停跳液的临床应用提供了实验依据。

We used Electron spin Resonance (ESR) spectroscopy to study the changes of the superoxide anion free radical on the myocardium of the isolated rat heart subjected to long-term ischemia at hypothermia and followed by 15s of reperfusion. The results showed that the signal intensity of the free radical of the superoxide anion decreased significantly as the temperature was lowered from 37℃ to 4℃, No significant change was noted within 4 hours while the hearts were protected by cardioplegia. After 240 min ischemia, all of the hearts in this group commenced beating automatically within 15s of reperfusion. In contrast, in the NS control group, the signal intensity increased 28. 6 ±10. 5% compared with that of 30 min ischemia/reperfusion (p<0.05), and after 240 min ischemia, none of the hearts of the control group began to beat within 15s of reperfusion After 240 min ischemia, in cardioplegia group, the reperfused injury of the ultrastructure was mild, whereas, in the NS control group, the following significant changes were noted: va uoius degeneration and obscured cristae within the mitochondria and marked expansion of the sarcoplasma reti-culum. Thus, we propose a bio-molecular mechanism of cardioplegia on heart preservation which could prove clinically useful in transplantation.