机构地区:[1]安徽医科大学第一附属医院麻醉科,合肥市230022
出 处:《中华麻醉学杂志》2013年第2期228-231,共4页Chinese Journal of Anesthesiology
基 金:安徽高校省级自然科学研究项目(KJ20122144)
摘 要:目的评价2型糖尿病因素对舒芬太尼后处理减轻大鼠心肌缺血再灌注损伤的影响。方法健康雄性清洁级sD大鼠,体重160~180g。采用高脂饲料喂养诱导胰岛素抵抗+腹腔注射链脲佐菌素方法制备2型糖尿病模型。取造模成功的大鼠18只,采用随机数字表法,将其分为3组(n=6):糖尿病假手术组(DM—S组)、糖尿病缺血再灌注组(DM—I/R组)、糖尿病舒芬太尼后处理组(DM—SP组)。另取健康大鼠18只,采用随机数字表法,将其分为3组(n=6):非糖尿病假手术组(NDM-S组)、非糖尿病缺血再灌注组(NDM—I/R组)、非糖尿病舒芬太尼后处理组(NDM—SP组)。采用左冠状动脉前降支下穿线,平衡30min,阻断30min,再灌注120min的方法制备心肌缺血再灌注损伤模型。NDM-SP组和DM-SP组于再灌注前5min经右颈静脉注射舒芬太尼1.0gg/kg。于缺血前即刻、缺血30min、再灌注120min(T1-3)时记录MAP、SP和HR,计算sP和HR乘积(RPP)。于再灌注120min时经右颈动脉采集血样,测定血浆cTnI浓度。处死后取心脏,测定心肌梗死体积。结果非糖尿病与糖尿病大鼠心肌缺血再灌注时MAP、RPP降低,血浆cTnI浓度升高,心肌发生梗死样改变。舒芬太尼后处理可减小非糖尿病大鼠心肌缺血再灌注时心肌梗死体积,降低血浆cTnI浓度,升高MAP和RPP,但对糖尿病大鼠心肌缺血再灌注时各指标无明显影响。结论2型糖尿病因素可阻碍舒芬太尼后处理对大鼠的心肌保护作用。Objective To investigate the effect of type 2 diabetes mellitus (DM) on the attenuation of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in rats. Methods Male pathogen-free Sprague-Dawley rats, weighing 160-180 g, were used in the study. A model for type 2 DM was established by the feeding of high-fat diet-induced insulin resistance and intraperitoneal streptozocin 35 mg/kg. DM was confirmed by blood glucose level ≥ 16.7 mmol/L one week after injection. Eighteen type 2 diabetic rats were randomly divided into 3 groups ( n = 6 each) : DM sham operation group (DM-S group) ; DM-I/R group; DM sufentanil postcondi- tioning group (DM-SP group). Another 18 healthy nondiabetic rats were chosen and randomly divided into 3 groups ( n = 6 each) : nondiabetes mellitus sham operation group (NDM-S group) ; nondiabetes mellitus I/R group (NDM- I/R group) ; nondiabetes mellitus sufentanil postconditioning group (NDM-SP group). Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery (after 30 min of equilibration) fol- lowed by 120 min of reperfusion. Sufentanil 1.0 μg/kg was injected via the right jugular vein 5 min before reperfu- sion in NDM-SP and DM-SP groups. MAP, SP and HR were recorded immediately before ischemia, at 30 min of ischemia and at 120 min of reperfusion and rate-pressure product (RPP) was calculated. Arterial blood samples were collected at 120 min of reperfusion for measurement of plasma cardiac troponin I (cTnI) concentration. Therats were then sacrificed for determination of the myocardial infract size. Results MAP and RPP were decreased, while the plasma cTnI concentration was increased during reperfusion in diabetic and nondiabetic rats. Sufentanil postconditioning decreased the myocardial infract size and plasma concentrations of cTnI, and increased MAP and RPP during reperfusion in nondiabetic rats, but had no effect on the parameters in diabetic rats. Conclusion Type 2 D
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