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Dynamic Expression of Myocardial β1-adrenoceptor and M2-muscarinic Acetylcholine Receptor in Stunning Myocardium of Rat Hearts

Author: ZhangHu
Tutor: GeJianJun；ZhouRuYuan；GeShengLin；LinMin
School: Anhui Medical University,
Course: Surgery
Keywords: Myocardial Stunning β1- adrenergic receptor M2- acetylcholine receptor
CLC: R363
Type: Master's thesis
Year: 2008
Downloads: 62
Quote: 0
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Abstract


Background myocardial stunning (Myocardial Stunning, MS), also known as myocardial dysfunction after ischemia, myocardial ischemia insufficient to cause short-term myocardial necrosis, but normal or near-normal blood flow is restored after reperfusion mechanical function The obstacles they need a few hours, a few days or even weeks to fully recover the pathological process. The myocardial stunning widespread clinical left ventricular dysfunction incidence and mortality increase one of the reasons. The large number of animal experiments and clinical studies have shown that myocardial stunning has already constituted a major pathophysiological basis of clinical heart surgery after heart transplantation common cardiac dysfunction occurred in recent years become a common problem in clinical cardiac surgery in the treatment process. Cardiopulmonary bypass blood catecholamines, angiotensin, vasopressin increased systemic vascular tension increases myofilament Ca 2 reduced susceptibility, and a lot of positive inotropic agents can only increase myocardial ATP is not conducive to the storage of ATP (adenosine triphosphate) depletion, easy to make the development of myocardial injury irreversible direction. Currently, many pathogenesis hypothesis in myocardial stunning, \Experimental findings of many domestic and foreign, that the existence of a variety of receptor systems, such as the β-adrenergic receptor, M-acetylcholine receptor, angiotensin receptors, adenosine receptors and receptor system in the myocardial tissue. Myocardial on these receptors are involved in regulating cardiac activity of the receptor, which was mainly play its regulation of cardiac activity on the myocardial membrane signal transduction system, plays an important role in maintaining normal cardiac function. However, change the number and function of the heart receptor system in the pathophysiology of myocardial stunning process and the mechanism of mutual adjustment between the receptor, few domestic and foreign studies on this aspect. With the in-depth study of the molecular biology and pharmacology mechanism of ischemic heart disease, in order to recognize the receptor research platform. The aim of the present experiment, respectively, at the cellular and genetic level observed Dayton suppression the myocardial receptor changes, to study the dynamic expression of the physiological function of the myocardial cell membrane receptors in myocardial stunning state to clarify MS pathogenesis an entirely new avenue of research, as well as myocardial stunning exploratory study receptor regulation, signal transduction mechanisms of myocardial function after drug intervention changes the research model. The first part of the method: to build a model of rat myocardial stunning, and clinical evaluation. 48 healthy adult male SD rats were randomly divided into the control group and the surgery group: operation group of the left anterior descending artery blocking 15min ischemia reperfusion time different, divided into five groups: ① reperfusion after 1 hour group; group four hours ② reperfusion; ③ The reperfusion after 8 team; 24 team after ④ reperfusion; group ⑤ reperfusion 72 hours after. The negative control group without the left anterior descending artery occlusion. Anesthetized SD rats by the left sternal 4 intercostal thoracotomy, exposed heart with needle slip line seam to take the left anterior descending coronary tighten the slip line to block, loosen the perfusion is restored, the establishment of the MS model . ECG was monitored throughout, and save it. The second part: β 1 - adrenergic receptor and M 2 - detection of acetylcholine receptors. Immunohistochemical method and RT-PCR (reverse transcription polymerase chain reaction) method to detect the stunning ventricular tissue by semi-quantitative analysis of the expression of two proteins in the myocardial tissue of the different groups were observed β < sub> 1 - the adrenaline receptor and M of 2 - acetylcholine receptor variation in myocardial stunning. (1), left ventricular anterior cyanosis and S-T segment elevation synchronous ECG showing QRS wave amplitude increases for blocking symbol of success. Anterior wall ischemia reperfusion District cyanosis disappeared synchronous ECG shows the S-T segment, QRS wave back down to normal. Of the stunning district ventricular muscle Histological examination of hematoxylin - eosin (HE) staining: no difference in the control group and the experimental group, the myocardial tissue of the heart in the light microscope, are normal myocardium structure. It can determine the success of the SD rat MS model making. (2) blocking SD rats left coronary anterior descending artery after 15 minutes to restore reperfusion β 1 -AR expression levels reperfusion time dependencies: in reperfusion sharp rise 1 hour decreased gradually returned to normal levels after 72 hours, and reached a peak, compared with the control group, and other surgical group, there is a statistically significant difference (P <0.05); M 2 -AChR expression levels to a minimum 4 hours of reperfusion, compared with the control group, and other surgical group, a statistically significant difference (P <0.05), then gradually increased; to re- perfusion reached a peak with the control group, eight hours and 1,4 hours reperfusion group compared with a statistically significant difference (P <0.05), 24-hour decline with the control group, 72 hours after reperfusion 1,4,24 hour group compared began to increase (P <0.05). The β 1 -AR myocardial cells and M 2 -AchR content differences, which is significantly higher than the previous. Conclusion (1) SD rat model of myocardial stunning prepared successfully; () β 1 -AR and M 2 -AChR involved in the pathophysiological process of myocardial stunning.

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