Essay On Ischemic Preconditioning

Although it has been explored through numerous experiments, ischemic preconditioning is yet it to be fully understood. All we know for now through experimenting on rats, rabbits and pigs, as well as in human isolated myocytes and human muscle tissue, is that a brief episode of ischemia has been shown to protect the heart from more prolonged episodes of ischemia, reducing infarct size, attenuating the incidence, and severity of reperfusion-induced arrhythmias, and preventing endothelial cell dysfunction. Several reports indicate that this phenomenon may be a form of receptor-mediated cardiac protection and that the underlying intracellular signal transduction pathways involve activation of a number of protein kinases, including protein kinase
We could also use the terms ‘First’ and ‘Second’ windows of myocardial protection to refer to the ‘Classic’ and the ‘Delayed’, respectively. Unlike the early phase of preconditioning, which lasts 2 to 3 hours and protects against infarction but not against stunning, the late phase of preconditioning lasts 3 to 4 days and protects against both infarction and stunning, suggesting that it might have greater clinical relevance. There also is a great difference regarding the mechanisms of each type and the cellular changes that occur to the cardiomyocyte thereafter. The clinical differences between the two is attributed to their unique mechanistic
It mainly works through dilation of the coronaries and thus delivering more oxygen to the hypoxic myocytes. It also works through decreasing the cardiac demand by reducing inotropy. Upon ischemia, Adenosine levels markedly rise in myocardial interstitium. Likely due to a rise in myocardial utilization of ATP. The effects of Adenosine are differentiated through different subtypes or receptors. Mainly; A1, A2, A3. Blockade of adenosine A1 and A3, but not A2 receptors, almost completely diminishes the effect of preconditioning in rabbits[18]. Stimulation of the adenosine A1 receptor with either