Zhang W
Cardiovascular Institute and Fu Wai Hospital, CAMS, Beijing.
Zhonghua Xin Xue Guan Bing Za Zhi. 1993 Oct;21(5):300-3, 316-7.
Isolated perfused rat heart model was used to observe the protective effects of berbamine on myocardial ischemia/reperfusion injury. The hearts were remarkably injured by 40 min global ischemia followed by 20 min reperfusion. Berbamine could significantly improve heart function, prevent ventricular fibrillation, reduce CK release, preserve Na, K-ATPase activity, and reduce Na+ gain and K+ loss during ischemia and Ca2+ overload during reperfusion. With the use of low temperature ESR technique, we found that, in hearts subjected to 40 min ischemia and 15 sec reperfusion, oxygen-centered free radical signals became much more intense. In the presence of berbamine, these signals decreased. The results showed that berbamine could alleviate myocardial ischemia/reperfusion injury. This effect might be due to (1) preserved myocardial Na, K-ATPase activity and inhibition of sodium overload at the end of ischemia, which might further lead to attenuation of reperfusion-induced calcium overload, and (2) reduction of oxygen free radical generation during reperfusion.
采用离体灌注大鼠心脏模型观察小檗胺对心肌缺血/再灌注损伤的保护作用。心脏经40分钟全心缺血后再灌注20分钟，受到显著损伤。小檗胺可显著改善心脏功能，预防心室颤动，减少肌酸激酶释放，维持钠钾ATP酶活性，减少缺血期间的钠内流和钾外流以及再灌注期间的钙超载。应用低温电子自旋共振技术，我们发现，在经历40分钟缺血和15秒再灌注的心脏中，以氧为中心的自由基信号变得更为强烈。在小檗胺存在的情况下，这些信号减弱。结果表明，小檗胺可减轻心肌缺血/再灌注损伤。这种作用可能归因于：（1）维持心肌钠钾ATP酶活性并抑制缺血末期的钠超载，这可能进而导致减轻再灌注诱导的钙超载；（2）减少再灌注期间氧自由基的生成。
