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:《临床麻醉学杂志》2015年第9期891-895,共5页Journal of Clinical Anesthesiology
基 金:2013年度国家自然科学基金主任基金项目(批准号:81341014);2012年国自然青年基金院内培育计划(3101005002352)
摘 要:目的研究糖尿病因素取消舒芬太尼后处理对大鼠缺血后心肌保护炎症机制的影响。方法雄性SD大鼠采用腹腔注射链脲佐菌素55mg/kg的方法制备1型糖尿病模型。取健康大鼠和造模成功的1型糖尿病大鼠各30只,随机分为六组(n=10):非糖尿病假手术组(NDM-SHAM组)、非糖尿病缺血-再灌注组(NDM-IR组)、非糖尿病舒芬太尼后处理组(NDM-SP组)、糖尿病假手术组(DM-SHAM组)、糖尿病缺血-再灌注组(DM-IR组)和糖尿病舒芬太尼后处理组(DM-SP组)。结扎冠状动脉左前降支(LAD)30min、再灌注120min,建立大鼠心肌缺血-再灌注损伤模型,舒芬太尼后处理组于再灌注前5min予舒芬太尼1μg/kg股静脉注射。分别记录缺血前即刻、缺血30min和再灌注120min时的HR、MAP的心率收缩压乘积(RPP)。于再灌注120min时计算心肌梗死面积(IS)和检测血浆肌钙蛋白I(cTnI)、TNF-α、IL-6、IL-8和IL-10的浓度。结果与NDM-SHAM组比较,NDM-IR组和NDM-SP组再灌注120min HR明显减慢、缺血30min、再灌注120min MAP和RPP明显降低,血浆cTnI、IL-6、IL-8、IL-10和TNF-α浓度明显升高(P<0.05);与DM-SHAM组比较,缺血30min、再灌注120min DM-IR组、DM-SP组MAP和RPP明显降低,血浆cTnI、IL-6、IL-8、IL-10和TNF-α浓度明显升高(P<0.05)。与NDM-IR组比较,再灌注120min DM-IR组HR明显减慢,NDM-SP组的IS、IS/AAR明显减少(P<0.05),血浆cTnI、IL-6、IL-8和TNF-α浓度明显降低(P<0.05),IL-10浓度明显升高(P<0.05);与NDM-SP组比较,DM-SP组的IS/AAR明显升高(P<0.05),血浆cTnI、IL-6、IL-8和TNF-α浓度明显升高(P<0.05),IL-10浓度明显降低(P<0.05)。结论炎症机制参与了糖尿病因素取消舒芬太尼后处理对大鼠缺血后心肌保护炎症机制作用。Objective To investigate inflammatory mechanisms in diabetes abolishing cardio- protection of sufentanil against ischemia/reperfusion (IR) injury. Methods Thirty non-diabetic melli- tus (NDM) SD rats and 30 streptozotocin (55 mg/kg) induced type 1 diabetic mellitus (DM) SD rats were divided into 6 groups (n= 10 each): non-diabetic sham group (group NDM-SHAM), non-dia- betic IR group (group NDM-IR), non-diabetic sufentanil postconditioning (SP) group (group NDM- SP), diabetic sham group (group DM-SHAM), diabetic IR group (group DM-IR) and diabetic sufen- tanil postconditioning group (group DM-SP). All the rats were exposed to 30 min ischemia and 120 min reperfusion except sham group. Sufentanil postconditioning was performed 5 min before the onset of reperfusion by i. v. injection of sufentanil at the dose of 1μg/kg HR, MAP, RPP were recorded im- mediately before ischema, at 30 min of ischemia and at 120 min of reperfusion. At the end of the 120 min reperfusion, blood was collected from the carotid artery immediately before the heart was ex- cised. Plasma cTnI, TNF-α, IL-6, IL-8 and IL-10 concentrations were measured using ELISA kit. Hearts were collected to assess area at risk (AAR) and infarct size. Results Compared with group NDM-SHAM, HR at 120 min of reperfusion MAP and RPP at 30 min of ischemia and 120 min of reperfusion were decreased, plasma concentrations of cTnI, TNF-α, IL-6, IL-8 and IL-10 were in-creased in group NDM-IR and group NDM-SP(P〈0.05). Compared with group DM-SHAM, MAP and RPP at 30 min of ischemia and 120 min of reperfusion were decreased, plasma concentrations of cTnI, TNF-α, IL-6, IL-8 and IL-10 were increased in group DM-IR and group DM-SP(P〈0.05). Compared with group NDM-IR, IS and IS/AAR were decreased, plasma concentrations of cTnI, TNF-α, IL-6, IL-8 were decreased, HR at 120 min of reperfusion was decreased in group DM-IR (P〈0. 05), IL-10 was increased in group NDM-SP(P〈0.05). Compared with group NDM-SP,
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