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In a myocardial infarction, the cardiomyocytes are damaged to quite some extent, and much of it of the affected area may also be permanently unusable. However, after the advent of a naturally occurring or an artificially induced myocardial infarction in the cardiac tissue in experimental models, it has been reported that specific cellular mechanisms are activated that try to salvage the cardiomyocytes which lead to the expression of particular proteins. Signal transduction pathways are activated with specific genes being hyperactivated by different feedback control mechanisms. These paths are known as the Reperfusion Injury Salvage Kinase (RISK) routes, and one of the major proteins activated in these signaling cascades is Akt (also known as protein kinase B), instrumental in promoting cell survival and contributing towards protection of the myocardium. In the present experiment, adult rat hearts/primary ventricular myocytes were exposed to simulated ischemia/ hypoxia. It was done prior to administration of ipratropium at the onset of reperfusion/reoxygenation, and comparative study was made on the impacts of acetylcholine on the same concerning Akt in nonclinical models of simulated myocardial ischemia/reperfusion injury help of SDS PAGE and Western blotting.
Extracellular alterations are responses of the cells to their adaptive procedures to extracellular stimuli by their activation of signal transduction pathways which culminate in changes in gene expression. In the cardiomyocytes that are undergoing ischemia and ischemia/ reperfusion, there has been considerable attention drawn on the signaling pathways that have been activated in response to stress (Davidson et al., 2006). Thus, both whole hearts and isolated cardiac myocytes, ischemia/reperfusion has been shown to activate signaling cascades leading to the activation members of MAPK or mitogen-activated protein kinase (Mockridge et al., 2000)....