关键词: 缺灌损伤, 再灌损伤, 乳酸脱氢酶, 心律失常, 小鼠

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