摘要
目的探讨糖原合成激酶(GSK)3β抑制剂SB216763是否增强异氟醚(ISO)后处理对心肌缺血-再灌注损伤的保护作用。方法雄性新西兰白兔,体重2.5～3.0kg,将模型制备成功的48只白兔随机分为八组(n=6),缺血-再灌注组(A组);ISO0.5MAC组(B组)或1.0MAC组(C组);GSK3β抑制剂SB216763(SB)0.2mg/kg组(D组)或0.6mg/kg(E组);ISO+SB组(F组);SB+苍术苷(Atr)组(G组);ISO+SB+Atr组(H组)。于缺血前(基础值,T0)、缺血30min(T1)、再灌注30min(T2)、60min(T3)和120min(T4)时分别记录HR和MAP;再灌注结束时,TTC法染色心肌切片并计算心肌梗死面积的百分比。结果 T0时各组血液动力学指标差异无统计学意义。与T0时比较,各组T3、T4时HR明显减慢、T2～T4时MAP明显降低(P<0.05)。与A组比较,C组、E组和F组心肌梗死面积明显缩小(P<0.05)。苍术苷废除了E组和F组的保护作用。结论 GSK3β抑制剂能够增强异氟醚后处理对心肌缺血-再灌注损伤的保护作用,并且该过程经由线粒体通透性转化孔调控。
Objective To explore whether inhibition of glycogen synthase kinase 3 beta （GSK3β） enhances isoflurane postconditioning-induced protection against myocardial ischemia- reperfusion. Methods Forty-eight Male New Zealand white rabbits weighing from 2.5 to 3.0 kg were randomly assigned into 8 groups： ischemia-reperfusion group （group A） ; isoflurane group 0.5 or 1.0 minimum alveolar concentration （MAC, group B ro group C） ; the selective GSK inhibitor SB216763 （SB） 0. 2 mg/kg （group D） or 0.6 mg/kg （group E）; isoflurane plus SB group （group F）; atractyloside received SB group（group G） or isoflurane plus SB group （group H）. Heart rate （HR） and mean arterial pressure （MAP） were recorded before occlusion, 30 min after occlusion, 30 min, 1 h and 2 h after reperfusion. Infarction area size （IS） was defined by TTC staining at the end of reperfusion. Results However HR and MAP significantly decreased after reperfusion when compared with To （P〈0. 05）. Compared with group A,group C and group E and group F myocardial infarction area decreased （P 〈 0.05）. Atractyloside abolished protection induced by group E or group F. Conclusion GSK3β inhibition enhances isoflurane postconditioning-induced protection against ischemia-reperfusion via a mitochondrial permeability transition （mPTP）-dependent mechanism.
出处
《临床麻醉学杂志》
CAS
CSCD
北大核心
2012年第10期1010-1012,共3页
Journal of Clinical Anesthesiology
