[Ischemic preconditioning inhibits ischemia/reperfusion induced myocardial apoptosis in rabbits in vivo].
Xu Jm, Hu Dx, Chang Yt
Abstract
Xu Jm, Hu Dx, Chang Yt
Abstract
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.
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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.
Key concepts: DNA laddering, Ischemic preconditioning, Ischemia, Medicine, Apoptosis, In vivo, Myocardial infarction, Evans Blue