缺血预处理抑制缺血再灌注所致兔在体心肌细胞凋亡

目的：为探讨缺血预处理对缺血再灌注过程中心肌细胞凋亡的影响。方法：将24只新西兰白兔制成在体心肌缺血／再灌注模型，并随机分成假手术对照组（P组），缺血／再灌注对照组（IR组），缺血预处理组（IP组），结果：IP组心肌梗死面积与缺血面积的比率比IR组显著减少（P＜0．05）；凋亡指数IP组亦比IR组小（P＜0．01），IR组心肌DNA Ladder形成明显，IP组DNA Ladder模糊不清，结论：缺血预处理对缺血／再灌注损伤中心肌细胞凋亡具有抑制作用。

Ischemic preconditioning inhibits ischemia/reperfusion induced myocardial apoptosis in rabbits in vivo]

OBJECTIVE: To investigate the effects of ischemic preconditioning on myocardial apoptosis induced by ischemia/reperfusion. METHODS: Twenty four rabbits were randomly allocated to three groups(n = 8), pseudo-operation group(group P), ischemia/reperfusion group(group IR), and ischemic preconditioning group (group IP). Group IR and group IP were subjected to three hours of left anterior descending coronary artery occlusion followed by three hours of reperfusion. Ischemic preconditioning was achieved by three 5-minute cycles of ischemia, each followed by 5 minutes of reperfusion. Infarct size and area at risk were defined by dual staining with triphenyltetrazolium chloride and Evans blue dye. DNA laddering in the border zone myocardium of ischemic area at risk was revealed with agarose gel electrophoresis, and apoptosis index(AI) was obtained with flow cytometry. RESULTS: Infarct size, expressed as a percentage of the area at risk(IS:AR), was(60.8 +/- 10.8)% in group IR. Ischemic preconditioning reduced myocardial infarct size significantly to (33.1 +/- 4.9)% (P < 0.05). AI was (13.83 +/- 3.98)% in group IR, and were reduced significantly to (5.85 +/- 1.59)% in group IP(P < 0.01). DNA laddering indicative of fragmented DNA was clearly demonstrated in myocardial specimens sampled from the lateral border zones of the ischemic area at risk in group IR but were attenuated in group IP. CONCLUSION: It suggests that ischemic preconditioning inhibits the rabbit myocardial apoptosis induced by ischemia/reperfusion in vivo.