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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Antibiotics, Antineoplastic, Cardiomyopathies, Doxorubicin, Hydrogen Sulfide, Male, Mitochondria, Heart, Myocardium, Oxidative Stress, Rats, Rats, Wistar, Sulfides, Superoxide Dismutase.
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Does hydrogen sulfide regulate cardiac function and structure in adriamycin-induced cardiomyopathy? Context: 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. 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).
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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. Final Decision: yes