title: Hydrogen sulfide regulates cardiac function and structure in adriamycin-induced cardiomyopathy.
abstract: 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.
  
  
  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.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing, China.
authors.forename: Yu-Wen
authors.initials: YW
authors.lastname: Su
authors.forename: Chen
authors.initials: C
authors.lastname: Liang
authors.forename: Hong-Fang
authors.initials: HF
authors.lastname: Jin
authors.forename: Xiu-Ying
authors.initials: XY
authors.lastname: Tang
authors.forename: Wei
authors.initials: W
authors.lastname: Han
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Chai
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Zhang
authors.forename: Bin
authors.initials: B
authors.lastname: Geng
authors.forename: Chao-Shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Jun-Bao
authors.initials: JB
authors.lastname: Du
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects* / Q000494:pharmacology; D009202:Cardiomyopathies / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D004317:Doxorubicin / Q000009:adverse effects* / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000378:metabolism*; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013440:Sulfides / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000903:Antibiotics, Antineoplastic; D013440:Sulfides; D004317:Doxorubicin; D013482:Superoxide Dismutase; C025451:sodium bisulfide; D006862:Hydrogen Sulfide