异丙酚对离体大鼠缺血/再灌注心肌丙二醛和含水量的影响

Effects of propofol against myocardial MDA metabolism and water content after ischemia/reperfusion injury in isolated rat hearts

目的 :探讨异丙酚对离体大鼠缺血 /再灌注心肌丙二醛 (MDA)和水肿程度的影响。方法 :采用改良Langendorff离体大鼠心脏模型 ,将 2 4只大鼠随机分成 4组。正常对照组 :用K H液持续灌注 80min ;缺血 /再灌注模型组 :用K H液预灌 30min ,然后用4℃的St.Thomas停搏液使心脏停跳 ,常温下全心停灌 2 0min ,K H液再灌注 30min ;异丙酚组和异丙酚 +格列本脲组 :从预灌第 15min改用含相应药液的K H液灌注 ,停灌同缺血 /再灌注模型组 ,然后用含相应药液的K H液再灌注 30min。测定心肌含水量、MDA含量和冠脉流出液肌酸激酶 (CK)活性。结果 :缺血再灌注可使心肌含水量、MDA含量和CK活性明显增高 (P <0 .0 1) ,30 μmol·L- 1异丙酚能显著减轻上述损伤性变化 ,格列本脲对异丙酚的心肌保护作用无影响 (P >0 .0 5 )。结论 :心肌缺血 /再灌注可致心肌水肿 ,异丙酚减轻水肿作用与其抗氧化有关 ,而与ATP

AIM: To investigate the effect of propofol on myocardial malondialdehyde (MDA) metabolism and water content after ischemia/reperfusion injury in isolated rat heart with the modified Langredorff model. METHODS: Twenty four rats were randomly divided into four groups. Rat hearts were perfused with Krebs Henseleik(K H)in normal control group. In other three groups,a three phase protocal was performed: (1) 15-30 min preperfusion, (2) 20 min global normothermic(37 ℃)ischemia,and (3) 30 min reperfusion. Then the group P was treated with 30 μmol·L -1 propofol, the group P+G 30 μmol·L -1 propofol+10 μmol·L -1 glibenclamide before ischemia and throughout the experiment. Only K H buffer was perfused in the group I R. The content of water and MDA in myocardium and creatin kinase (CK) in the coronary effluent were measured. RESULTS: The recovery of hearts treated with propofol were better than that of group I R, indicated by lower content of water, MDA and CK level (P< 0.01 ). No statistically significant differences were observed between group P and group P+G (P> 0.05 ). CONCLUSION: Propofol can relieve myocardial edema by scavenging oxygen free radical and the mechanism is related to open of KATP channels.