Abstract: By means of Langendorff method, isolated mouse heart was perfused with Krebs-Hensleit (K-H) buffer solution. After 10 min equilibrium, the heart underwent global ischemia of three different duration followed by 10 min reperfusion. During the first 5 min of reperfusion, coronary effluents were collected in accordance with given sequence, in order to analyze Lactate Dehydrogenase (LDH) activity U/L as an index of cellular damage induced by ischemicreperfusion. Ischemia, classified into threegroups (5 min, 10 min, and 15 min), caused a biphasic LDH release. The first one, which represented mainly ischemic injury, appeared in the first 15 s of reperfusion, and had higher value than that of control. The activities of LDH release were (55.4±3.8), (86.8±5.4), and (96.2±6.8)U/L, for the above 3 groups, respectively. The second peak appeared in 180 to 240 s of reperfusion represented mainly reperfusion injury, and was lower than that of the first peak, but higher than controlvalue. Arrhythmias, e.g., premature ventricular contraction (PVC) and ventricular tachycardia (VT) were observed during 5 min reperfusion period. The numbers of PVC were 187±17, 217±10, and 244±14, whereas the duration of VT was (10±2) s, (22±3) s, and (24±2) s, for above 3 groups, respectively. Normal sinus rhythm time (NSRT) during early reperfusion period of the above 3 groups were measured to (214±SD29), (196±SD31) and (183±SD24) s, respectively. In this study and experimental ischemiareperfusion model indicated by LDH release has been the first established mouse heart at our laboratory. This model had provided convenient approach and new possibilities for further investigation and protection of cardiac ischemia-reperfusion injury.

Key words: ischemia (noperfusion) injury, reperfusion injury, lactate dehydrogenase, arrhythmia, mouse

摘要： 离体小鼠心脏，用Langendorff法灌流，平衡10min后全心缺灌，于再灌期最初5min内按一定时间顺序收集冠脉流出液，测定乳酸脱氢酶(LDH)的活性浓度(U/L)，作为心肌细胞损伤的指标。实验分3组，分别采取不同的缺灌时间：5min，10min和15min。平衡期LDH释放对照值3组分别为(7.8±0.8)、(7.9±0.7)和(7.6±0.7)U/L。缺灌期即开始LDH的大量释放，随缺灌时间加长而递增。再灌期，3组LDH均呈现双相释放，第Ⅰ峰出现于再灌开始15s，峰值极高，分别为：5min缺灌组：(55.4±3.8)U/L；10min组：(86.8±5.4)U/L，15min组：(96.2±6.8)U/L，均与各自平衡期对照值差异显著(p<0.001)。该峰升降迅速，主要反映缺灌对心肌的损伤。第Ⅱ峰出现于再灌早期第180～240s之间，峰值较低。3组分别为(15.4±2.0)、(17.3±1.6)和(15.9±1.4)U/L。3组之间，除第Ⅰ峰峰值5min组与10min组、15min组差异显著外，其余各点均无显著差异。此外，统计了再灌期5 min内出现的心律失常，有室性早搏(PVC)和室速(VT)。PVC次数在上述3组中分别为187±17，217±10和244±14。VT所占时间在这3组中分别为(10±2)s，(22±3)s，(24±2)s。再灌期正常窦性节律时间(NSRT)分别为(214±SD29)s(SD为标准差)，(196±SD24)s和(183±SD24)s。实验首次用小鼠离体心脏建立了一个以心肌LDH释放为指标的实验模型，为深入研究缺血再灌对心脏损伤及其防护提供了方便和新的可能性。

关键词: 缺灌损伤, 再灌损伤, 乳酸脱氢酶, 心律失常, 小鼠