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
发布时间：2018-08-03 10:18
【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(P0.05);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(P0.05),LVEDP和血浆中CK-MB含量均明显升高(P0.05)。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(P0.05),LVEDP和血浆中CK-MB含量均明显降低(P0.05),其中高剂量组较低剂量组变化更明显(P0.05)。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]:Aim: to investigate the effects of acardipine on myocardial energy metabolism in canine models of (CPB) myocardial ischemia reperfusion injury induced by cardiopulmonary bypass (CPB). Methods: dogs were randomly divided into control group (n = 6), model group (n = 6), acardidine low group (n = 6) and high dose group (n = 6). All dogs were treated with CPB. The MIRI model was established in all dogs except the control group and the St.Thomas cardioplegic solution containing the corresponding drugs was infused after 60 min of aortic occlusion. Myocardial glucose and free fatty acid (FFA) uptake rate, creatine kinase isoenzyme (CK-MB) content in venous sinus plasma and adenosine triphosphate (ATP) content in mitochondria were measured and calculated before and after reperfusion for 1560 ~ 90 min, respectively. Left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP);) were analyzed to detect the expression of adenylate activated protein kinase (AMPK) mRNA) and phosphorylated AMPK (p-AMPK) protein in myocardial tissue. Results: there was no significant difference in all indexes before bypass in each group (P0.05). Myocardial glucose uptake rate and ATP content in three time points of the model group and each administration group, the expression of p-AMPK protein and LVSP in AMPK mRNA were significantly decreased (P0.05) and the content of CK-MB in plasma was significantly increased (P0.05). Compared with the model group, Myocardial glucose uptake rate and FAA uptake rate and ATP content in three time points of each administration group, the expression of AMPK mRNA and the expression of p-AMPK protein and LVSP were significantly increased (P0.05) and the content of CK-MB in plasma decreased significantly (P0.05), especially in the high-dose group compared with the low-dose group (P0.05). Conclusion: acardipine can promote the phosphorylation of AMPK, increase the uptake of glucose and FFA in myocardium, increase ATP in myocardial mitochondria and alleviate MIRI after CPB.
【作者单位】： 遵义医学院附属医院心血管外科;新乡医学院第一附属医院心血管外科;
【基金】：国家自然科学基金资助项目(No.81560058、81360035) 贵州省科技计划项目(No.黔科合SZ字[2014]3022号) 贵州省科技合作计划项目(No.黔科合LH字[2015]7507号)
【分类号】：R965
本文编号：2161432
[Abstract]:Aim: to investigate the effects of acardipine on myocardial energy metabolism in canine models of (CPB) myocardial ischemia reperfusion injury induced by cardiopulmonary bypass (CPB). Methods: dogs were randomly divided into control group (n = 6), model group (n = 6), acardidine low group (n = 6) and high dose group (n = 6). All dogs were treated with CPB. The MIRI model was established in all dogs except the control group and the St.Thomas cardioplegic solution containing the corresponding drugs was infused after 60 min of aortic occlusion. Myocardial glucose and free fatty acid (FFA) uptake rate, creatine kinase isoenzyme (CK-MB) content in venous sinus plasma and adenosine triphosphate (ATP) content in mitochondria were measured and calculated before and after reperfusion for 1560 ~ 90 min, respectively. Left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP);) were analyzed to detect the expression of adenylate activated protein kinase (AMPK) mRNA) and phosphorylated AMPK (p-AMPK) protein in myocardial tissue. Results: there was no significant difference in all indexes before bypass in each group (P0.05). Myocardial glucose uptake rate and ATP content in three time points of the model group and each administration group, the expression of p-AMPK protein and LVSP in AMPK mRNA were significantly decreased (P0.05) and the content of CK-MB in plasma was significantly increased (P0.05). Compared with the model group, Myocardial glucose uptake rate and FAA uptake rate and ATP content in three time points of each administration group, the expression of AMPK mRNA and the expression of p-AMPK protein and LVSP were significantly increased (P0.05) and the content of CK-MB in plasma decreased significantly (P0.05), especially in the high-dose group compared with the low-dose group (P0.05). Conclusion: acardipine can promote the phosphorylation of AMPK, increase the uptake of glucose and FFA in myocardium, increase ATP in myocardial mitochondria and alleviate MIRI after CPB.
【作者单位】： 遵义医学院附属医院心血管外科;新乡医学院第一附属医院心血管外科;
【基金】：国家自然科学基金资助项目(No.81560058、81360035) 贵州省科技计划项目(No.黔科合SZ字[2014]3022号) 贵州省科技合作计划项目(No.黔科合LH字[2015]7507号)
【分类号】：R965
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