乳化异氟醚预处理对大鼠心肌缺血再灌注损伤时炎性反应的影响  

Effects of preconditioning with emulsified isoflurane on inflammatory response to myocardial ischemiareperfusion injury in rats

作　　者：胡朝阳[1] 刘进[1] 

机构地区：[1]610041成都市,四川大学华西医院麻醉科

出　　处：《中华麻醉学杂志》2012年第5期589-592,共4页Chinese Journal of Anesthesiology

基　　金：国家自然科学基金（30901412）

摘　　要：目的评价乳化异氟醚预处理对大鼠心肌缺血再灌注损伤时炎性反应的影响。方法健康sD大鼠40只，体重250—280g，雌雄各半，采用随机数字表法，将大鼠随机分为假手术组（s组）、心肌缺血再灌注损伤组（IR组）、脂肪乳组（I组）和乳化异氟醚组（EI组），每组10只。采用结扎左冠状动脉前降支30min，再灌注180rain的方法制备大鼠心肌缺血再灌注损伤模型。S组、IR组、I组和EI组于尾静脉分别输注0．9％生理盐水、0．9％生理盐水、30％脂肪乳和乳化异氟醚2ml／kg（液态异氟醚体积比为8％），给药时间30min，停止给药后30rain制备模型。于再灌注180min时抽取心脏血后处死大鼠取心脏，采用TIC染色法测定心肌梗死面积，放射免疫法测定血浆肿瘤细胞坏死因子α（TNF—α）浓度，免疫组化法检测缺血心肌细胞核因子-κBp65（NF—κBp65）和细胞黏附分子-1（ICAM-1）的表达。结果与s组比较，其余3组心肌梗死面积增加，血浆TNF—α浓度升高，心肌NF—κBp65和ICAM一1表达上调（P〈0．05）；与IR组和I组比较，EI组心肌梗死面积减少，血浆TNF—α浓度降低，心肌NF—κBp65和ICAM-1表达下调（P〈0．05）。结论乳化异氟醚预处理可减轻大鼠心肌缺血再灌注损伤，其机制可能与抑制心肌细胞NF—κB和ICAM-1表达，减轻炎性反应有关。Objective To investigate the effects of preconditioning with emulsified isoflurane （eISO） on inflammatory response to myocardial isehemia-reperfusion （I/R） injury in rats. Methods Forty SD rats of both sexes weighing 250-280 g were randomly allocated into 4 groups （ n = 10 each） ： group Ⅰ sham operation （S） ; group Ⅱ myocardial I/R ＋ normal saline （NS） ; group Ⅲ I/R ＋ eISO and group Ⅳ I/R ＋ 30% intralipid （IL） （vehicle for elSO） . Myocardial isehemia was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 180 min reperfusion. NS, 30% intralipid and eISO 2 ml/kg were infused iv over 30 min at 30 min before myocardial isehemia in groups Ⅱ, Ⅲ and Ⅳ respectively. The animals were killed at the end of 180 rain reperfusion. Their hearts were removed for determination of infarct size and myocardial NF-κB p65 and ICAM-1 expression （by immnno-histochemistry） and plasma concentration of TNF-α （by radioimmunoassay）. Results Myocardial I/R induced myocardial infarct and significantly increased plasma TNF-α concentration and myocardial ICAM-1 and NF-κB p65 expression in group Ⅱ, Ⅲ and Ⅳ as compared with sham operation group （ Ⅰ ） . Plasma TNF-α concentration and myocardial ICAM-1 and NF-κB p65 expression were significantly lower in group Ⅲ （elSO） than in group Ⅱ and Ⅳ . Conclusion Down-regulation of myocardial NF-κB and ICAM-1 expression and inhibition of inflammatory response are involved in the mechanism by which preconditioning with iv elSO protects against myocardial I/R injury.

关 键 词：异氟醚 乳化剂 心肌再灌注损伤 NF—κB 细胞黏附分子 

分 类 号：R965[医药卫生—药理学]