阿卡地新对体外循环心肌缺血再灌注损伤模型犬心肌能量代谢的影响
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篇名: 阿卡地新对体外循环心肌缺血再灌注损伤模型犬心肌能量代谢的影响
TITLE:
摘要: 目的:探讨阿卡地新对体外循环(CPB)心肌缺血再灌注损伤(MIRI)模型犬心肌能量代谢的影响。方法:将犬随机分为对照组、模型组和阿卡地新低、高剂量组(0.8、3.2 mg/kg),每组6只。所有犬行CPB术,除对照组外,其余各组犬建立MIRI模型,并于主动脉阻断60 min后灌注含相应药物的St.Thomas心脏停搏液。分别于转流前和再灌注15、60、90 min时检测并计算心肌葡萄糖和游离脂肪酸(FFA)摄取率、静脉窦血浆中肌酸激酶同工酶(CK-MB)含量、线粒体中三磷酸腺苷(ATP)含量;分析左心室收缩压(LVSP)和左心室舒张末期压(LVEDP);检测心肌组织中腺苷酸活化蛋白激酶(AMPK) mRNA表达和磷酸化AMPK(p-AMPK)蛋白表达。结果:各组犬转流前的所有指标差异均无统计学意义(P>0.05);转流后,与对照组比较,模型组和各给药组犬3个时间点的心肌葡萄糖摄取率、FAA摄取率、ATP含量、AMPK mRNA表达、p-AMPK蛋白表达和LVSP均明显降低(P<0.05),LVEDP和血浆中CK-MB含量均明显升高(P<0.05)。与模型组比较,各给药组犬3个时间点的心肌葡萄糖摄取率、FAA摄取率、ATP含量、AMPK mRNA表达、p-AMPK蛋白表达和LVSP均明显升高(P<0.05),LVEDP和血浆中CK-MB含量均明显降低(P<0.05),其中高剂量组较低剂量组变化更明显(P<0.05)。结论:阿卡地新可促进AMPK磷酸化,有助于心肌葡萄糖和FFA的摄取,促使心肌线粒体中ATP增加,有助于减轻CPB术后MIRI。
ABSTRACT: OBJECTIVE: To explore the effects of acadesine on myocardial energy metabolism of model dogs with myocardial ischemia-reperfusion injury (MIRI) after cardiopulmonary bypass (CPB). METHODS: Dogs were randomly divided into control group, model group, acadesine low-dose, high-dose groups (0.8, 3.2 mg/kg), 6 in each group. All dogs received CPB. Except for control group, dogs in other groups were reduced for MIRI model, and perfused St.Thomas cardiac cardioplegia lipid containing relevant drugs 60 min after main artery block. The uptake rates of myocardial glucose and free fatty acid (FFA), creatine kinase isoenzyme (CK-MB) concent in venous sinus plasma and adenosine triphosphate (ATP) content in mitochondria were detected and calculated before bypass and after 15, 60, 90 min of reperfusion. Left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were analyzed, and mRNA expression of adenylate-activated protein kinase (AMPK) and protein expression of phosphorylated AMPK (p-AMPK) in myocardial tissue were detected. RESULTS: Before bypass, all indexes in each group had no statistic significances (P>0.05). After bypass, compared with control group, uptake rates of myocardial glucose and FAA, ATP content, mRNA expression of AMPK and protein expression of p-AMPK and LVSP in 3 time points in model group and each administration group were obviously decreased (P<0.05); LVEDP and CK-MB concent in plasma were obviously increased (P<0.05). Compared with model group, uptake rates of myocardial glucose and FAA, ATP content, mRNA expression of AMPK and protein expression of p-AMPK and LVSP in 3 time points in each administration group were obviously increased (P<0.05); LVEDP and CK-MB concent in plasma were obviously decreased (P<0.05); and high-dose group showed more obvious change than that of low-dose group (P<0.05). CONCLUSIONS: Acadesine can promote the AMPK phosphorylation, contribute to the myocardial glucose and FFA uptake to promote the increase of ATP in myocardial mitochondria and relieve MIRI after CPB.
期刊: 2017年第28卷第28期
作者: 张登沈,梁贵友,刘达兴,张建,王峰,刘晓晨
AUTHORS: ZHANG Dengshen,LIANG Guiyou,LIU Daxing,ZHANG Jian,WANG Feng,LIU Xiaochen
关键字: 阿卡地新;体外循环;犬;心肌缺血再灌注损伤;心肌能量代谢
KEYWORDS: Acadesine; Cardiopulmonary bypass; Dogs; Myocardial ischemia-reperfusion injury; Myocardial energy metabolism
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