Myocardial ischemia is a condition in which the coronary blood flow to the myocardium is abridged resulting in deficient oxygen and nutrients supply to the heart. Reperfusion to an ischemic myocardium often results in lethal myocardial injury. The brief episodes of ischemia and reperfusion given before prolonged ischemia and reperfusion denotes preconditioning. In this review we have discussed the phenomenon of cardioprotection against ischemia reperfusion injury with various cardioprotective mechanisms contributed by ischemic preconditioning. Classical and delayed preconditioning has been described in this review. The protective effects of ischemia/perfusion cycles are evident within minutes after the insult and persist for 2-3 hours known as classical preconditioning or first window of protection (FWOP). The apparent approximately 24 hours after initial preconditioning and it can persist for up to 72 hours is known as delayed preconditioning or second window of protection (SWOP). Ischemic preconditioning activates some pharmacological cardioprotective endogenous or exogenous triggers such as mitochondrial K-ATP channel, adenosine, bradykinin, acetylcholine, nitric oxide (NO) and activation of protein kinase-c (PKC) and inhibition of mitochondrial permeability transition pore (MPTP). In this review, we have critically discussed the various triggers and their signalling pathways involved in the modulation of cardioprotective potential of ischemic preconditioning.
