| Part 1 A rat model of coronary artery ligation induced heart failureObjective: The purpose of the present study was to establish a effective rat model 0f coronary artery ligation induced heart failure.Methods: Experimental rats were randomly divided into normal control group(NC group),model group,Propranolol intervention group,and Metoprolol intervention group.Heart failure rat model was conducted by coronary artery ligation.Rats in the NC group only had a thoracotomy while the remaining three groups were ligated the anterior descending coronary artery all.The Propranolol intervention group and the Metoprolol intervention group were given drugs by weight.Rats in the NC group and the model group were given the same amount of saline.After the model was completed,Doppler echocardiography was used to detect the heart function of each group.Results: Compared with the NC group,Left ventricular ejection fractions(EF)and Left ventricular fractional shortening(FS)of the rats in the model group,the Propranolol intervention group and the Metoprolol intervention group all decreased(p<0.05);Interestly,compared with the model group,the values of EF and FS in the Propranolol intervention group and the Metoprolol intervention group were significantly higher(p<0.05)Surprisingly,the rats in the model group,the propranolol intervention group and the metoprolol intervention group exhibited different degrees of cardiac enlargement and cardiac hypertrophy.Conclusion: Heart failure rat model was successfully conducted by coronary artery ligation.;β renergic blockers can improve myocardial remodeling in rats.Part 2 Effect of AKAP5-mediated β-ARs on the occurrence of arrhythmias in rats with heart failure after myocardial infarctionObjective: The purpose of the present study was to observe the changes of expression of A kinase-anchored protein 5(AKAP5)and β-adrenergic receptor(β-ARs)in heart failure rats;To explore the effect of AKAP5 and β-ARs on the occurrence rate of arrhythmia in heart failure rats and its possible mechanism.Methods: Procedural electrical stimulation was used to observe the occurrence of arrhythmia in each group;The m RNA a nd protein expression of AKAP5,β1-AR and β2-AR in each group were detected by q PCR and Western-blot,respectively.Results: Compared with the NC group,the occurrence rate of arrhythmia in the model group,the Propranolol intervention group and the Metoprolol intervention group was increased significantly.Differently,compared with the model group,the occurrence rate of arrhythmia was reduced significantly in the Propranolol intervention group and the Metoprolol intervention group.Compared with the NC group,the expression of AKAP5 m RNA and protein in the model group was decreased(P<0.05).While compared with the model group,the expression of AKAP5 m RN A and protein was significantly higher in the Propranolol intervention group and the Metoprolol intervention group(P<0.05).Compared with the NC group,the expression of β1-AR m RNA and protein in the model group was decreased(P<0.05).However,compared with the model group,the levels of β1-AR m RNA and protein in the Propranolol intervention group and the Metoprolol intervention group was increased(P<0.05).While when we testing the m RNA and protein levels of β2-AR,there was no different between model group and NC group(P>0.05);Similarly,compared with the model group,the β2-AR m RNA and protein levels in the propranolol intervention group and the Betaloc intervention group also had no significant difference(P>0.05)Conclusion: β adrenergic receptor blockers can reduce the occurrence rate of arrhythmia in heart failure rats;AKAP5 may be involved in the regulation of arrhythmia by β-ARs in heart failure rats. |
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