Effect of Sodium Thiosulfate Postconditioning on Ischemia-Reperfusion Injury Induced Mitochondrial Dysfunction in Rat Heart.

The recent research on the therapeutic applications of sodium thiosulfate (STS) has gained importance in the treatment of cardiovascular diseases. Progressively through the present work, we have demonstrated that postconditioning of isolated rat heart subjected to ischemia-reperfusion injury using STS had preserved the mitochondrial structure, function, and number. Heart comprising of two mitochondrial subpopulations interfibrillar (IFM-involved in contractile function) and subsarcolemmal (SSM-involved in metabolic function), STS postconditioning imparted a state of hypometabolism to SSM, thereby reducing the metabolic demand of the reperfused heart. The IFM, on the other hand, provided the energy required to maintain contraction. Moreover, the hypometabolic state induced in SSM can lower the free radical release in addition to STS innate ability to act as an antioxidant and radical scavenger, all of which collectively provided cardioprotection. Therefore, drugs targeting IFM specifically or those reducing the energy demand for SSM can be suitable targets for myocardial ischemia-reperfusion injury.