【摘要】：目的:探討阿卡地新對體外循環(huán)(CPB)心肌缺血再灌注損傷(MIRI)模型犬心肌能量代謝的影響。方法:將犬隨機(jī)分為對照組、模型組和阿卡地新低、高劑量組(0.8、3.2 mg/kg),每組6只。所有犬行CPB術(shù),除對照組外,其余各組犬建立MIRI模型,并于主動脈阻斷60 min后灌注含相應(yīng)藥物的St.Thomas心臟停搏液。分別于轉(zhuǎn)流前和再灌注15、60、90 min時檢測并計算心肌葡萄糖和游離脂肪酸(FFA)攝取率、靜脈竇血漿中肌酸激酶同工酶(CK-MB)含量、線粒體中三磷酸腺苷(ATP)含量;分析左心室收縮壓(LVSP)和左心室舒張末期壓(LVEDP);檢測心肌組織中腺苷酸活化蛋白激酶(AMPK)mRNA表達(dá)和磷酸化AMPK(p-AMPK)蛋白表達(dá)。結(jié)果:各組犬轉(zhuǎn)流前的所有指標(biāo)差異均無統(tǒng)計學(xué)意義(P0.05);轉(zhuǎn)流后,與對照組比較,模型組和各給藥組犬3個時間點(diǎn)的心肌葡萄糖攝取率、FAA攝取率、ATP含量、AMPK mRNA表達(dá)、p-AMPK蛋白表達(dá)和LVSP均明顯降低(P0.05),LVEDP和血漿中CK-MB含量均明顯升高(P0.05)。與模型組比較,各給藥組犬3個時間點(diǎn)的心肌葡萄糖攝取率、FAA攝取率、ATP含量、AMPK mRNA表達(dá)、p-AMPK蛋白表達(dá)和LVSP均明顯升高(P0.05),LVEDP和血漿中CK-MB含量均明顯降低(P0.05),其中高劑量組較低劑量組變化更明顯(P0.05)。結(jié)論:阿卡地新可促進(jìn)AMPK磷酸化,有助于心肌葡萄糖和FFA的攝取,促使心肌線粒體中ATP增加,有助于減輕CPB術(shù)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.
【作者單位】： 遵義醫(yī)學(xué)院附屬醫(yī)院心血管外科;新鄉(xiāng)醫(yī)學(xué)院第一附屬醫(yī)院心血管外科;
【基金】：國家自然科學(xué)基金資助項目(No.81560058、81360035) 貴州省科技計劃項目(No.黔科合SZ字[2014]3022號) 貴州省科技合作計劃項目(No.黔科合LH字[2015]7507號)
【分類號】：R965

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