ABSTRACT
OBJECTIVE： To investigate the effects of adiponectin （APN） on the expression of myocardial AMPK in myocardial insulin resistance （IR） model dogs during cardiopulmonary bypass （CPB）. METHODS： Totally 24 dogs were randomly divided into control group， model group， APN group （36 μg/kg）， AMPK inhibition group （APN 36 μg/kg+AMPK inhibitor compound C 0.5 mg/kg）， with 6 dogs in each group. All dogs underwent CPB； except for control group without medicine， CPB myocardial IR model were established in other groups， and perfused with St.Thomas cardiac cardioplegia lipid no medicine or containing relevant drugs after main artery block. Coronary sinus blood and carotid artery blood samples were collected before bypass and after 15， 90 min reperfusion following 60 min myocardial ischemia. Left ventricular apical tissue was taken， and the uptake rate of myocardial glucose and insulin resistance index （IRI） were determined and calculated； the changes of myocardial injury indexes （cTnT concentration） and cardiac function indexes （LVSP， +dp/dtmax） were monitored. The level of p-AMPK was detected. RESULTS： There was no statistical significance in above indexes of dogs before bypass （P＞0.05）. Compared with control group， the rate of myocardial glucose uptake， the levels of LVSP， +dp/dtmax and p-AMPK in model group were decreased significantly after 15， 90 min reperfusion （P＜0.05）， and the concentrations of IRI and cTnT were increased significantly （P＜0.05）. Compared with model group， the rate of myocardial glucose uptake， LVSP， +dp/dtmax and p-AMPK were increased significantly in APN group and AMPK inhibitor group （P＜0.05）， while the concentrations of IRI and cTnT were decreased significantly （P＜0.05）； moreover， the effect of APN group was better than that of AMPK inhibitor group （P＜0.05）. CONCLUSIONS： APN can promote myocardial glucose uptake and metabolism， and contribute the recovery of cardiac function， the mechanism of which may be associated with increasing the activity of AMPK.
ABSTRACT
Objective This study was carried out to investigate the effect of myocardial insulin resistance on expression of p38 mitogen-activated protein kinase (MAPK) in ischemic heart failure in rat.Methods Male sprague-dawley rats were subjected either to ligation of the left anterior descending artery (LAD) (n =24) or to sham operation (n =24).After two weeks,cardiac size and function were determined by echocardiography.Glucose and fatty acid (FAO) oxidation rates as well as insulin response were measured in the isolated working heart.The protein expression of p38MAPK was evaluated by Western blotting.Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction ＜0.50).The basal glucose oxidation was preserved,but the fatty acid oxidation was significantly reduced.Insulin effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation.The protein expression of p38MAPK in infracted hearts wasfisigni cantly reduced(P＜0.05).Condusion Myocardial infarction in rats caused partial insulin resistance at the level of substrate oxidation,which was associated with cardiac contractile dysfunction and the expression of p38MAPK.