Effect Of Simulated Ischemic Preconditioning On Connexin And I_Cl,swell In Primarily Cultured Sinoatrial Node Cells Of Neonatal Rat

Background and objectiveSick sinus syndrome (SSS) is a common cardiovascular disease which is greatly harmful to human health. To elucidate the pathogenesis of SSS and find out the possible measures of prevention and radical cure is always an important part of the angiocardiopathy study. In the previous study, we have found that simulated ischemia/reperfusion(I/R) could cause structural and functional damages to sinoatrial node cells in vivo and in vitro, leading to electrophysiological disturbance by affecting the regular rhythm and frequency.Myocardium ischemic preconditioning(IP), which is considered as the most powerful protective inherence found in almost all kinds of animals and human, can relief various kinds of cardiac damages caused by I/R. But the signal transduction of IP is very complicated and redundant, only a little has been known about its protective mechanism and the study of effect of IP on the sinoatrial node cells is rarely seen. Connexin has also been given more and more concern about it's contribution to the IP recently due to an end effector in IP. Substantial evidence indicates that swell-induced chloride current (ICl,swell) contributes to cardiac electrical activity and cellular volume regulation in both physiologic and pathophysiologic situations. Swelling occurs during ischemia and reperfusion, and it is postulated that this activates ICl,swell. Studies have revealed ICl,swell is essential for the IP due to a regulating role in mechanoelectrical feedback of myocardium. Based on the primarily cultured sinoatrial node pacemaker cells in neonatal rat, the purpose of our investigation is to observe the effects of simulated IP on the changes of cell viability after severe simulated I/R, detect the role of connexins in IP and discuss the mechanism, observe whether ICl,swell is present in primarily cultured sinoatrial node cells in neonatal rat, and discuss the signaling cascades participated in its activation, providing experimental evidence for further prevention of sinoatrial node injuries caused by I/R.