Hydrogen sulfide regulates cardiac function and structure in adriamycin-induced cardiomyopathy.

Background: The present study was designed to investigate if hydrogen sulfide (H2S), a novel gasotransmitter, might have a regulatory effect on cardiac function and structure, as well as oxidative stress, in adriamycin (ADR)-induced cardiomyopathy. Methods and Results: Hemodynamic measurements, histopathological examination and stereological ultrastructural analysis of mitochondria in ADR-treated rats showed characteristics of cardiomyopathy with remarkable greater size and smaller number of cardiomyocytic mitochondria and a significantly low H2S content in plasma and myocardium, but increased levels of thiobarbituric acid reactive substance (TBARs) and decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in plasma and myocardium compared with controls (P < 0.01). However, administration of the H2S donor, NaHS, markedly improved cardiac function, as demonstrated by elevated left ventricular developed pressure (+/-LVdp/dtmax; P < 0.01) with ameliorated morphological alterations in the myocardium. Myocardial TBARs content decreased, whereas the activities of SOD and GSH-Px increased (P < 0.01 and P < 0.05, respectively). Conclusions: Downregulation of endogenously-generated H2S is probably involved in the pathogenesis of ADR-induced cardiomyopathy, whereby H2S reduces lipid peroxidation, increases antioxidation, and inhibits oxidative stress injury. (Circ J 2009; 73: 741-749)