title: Hydrogen sulphide attenuates renal and cardiac injury after total hepatic ischemia and reperfusion.
abstract: BACKGROUND
  There are few studies that focus on the important organs injuries induced by total hepatic ischemia and reperfusion (THIR), which is a key to save the lives of hepatic surgery patients. We evaluated changes in the hydrogen sulphide production system and injuries to the heart and kidney. The aim of this study was to assess whether sodium hydrosulphide (NaHS) has protective effects against THIR injury.
  
  
  METHODS
  Under anaesthesia of the Wistar rats, the hepatic artery, the portal vein, and the inferior vena cava above and below the liver were clamped with nontraumatic arterial clamps. Hepatic reperfusion was achieved by removing the clamps.
  
  
  RESULTS
  Hydrogen sulphide production system was down-regulated after THIR, which caused severe damage to the heart and kidney, apart from the liver. In treated animals, CK-MB and LDH were lower by 26.9% and 14.2% (P < 0.05), respectively. The kidney showed similar change. Hematoxylin and eosin staining demonstrated fewer injuries in NaHS treated animals. The results indicated that the damage was abolished by exogenous NaHS.
  
  
  CONCLUSIONS
  The observed protection of exogenous NaHS is associated with reduced myocardial and renal inflammation and oxidative potential after THIR. The current results suggest that hydrogen sulphide is protective during the evolution of THIR and that either direct hydrogen sulphide administration or the modulation of endogenous production may be of clinical importance.
authors.affiliation: First Department of Comprehensive Surgery, South Building, PLA General Hospital of China, Beijing, China.
authors.forename: Yawei
authors.initials: Y
authors.lastname: Chen
authors.forename: Zhenhua
authors.initials: Z
authors.lastname: Liu
authors.forename: Xiaohua
authors.initials: X
authors.lastname: Xie
mesh_terms: D000818:Animals; D015815:Cell Adhesion Molecules / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006499:Hepatic Artery / Q000502:physiology; D006862:Hydrogen Sulfide / Q000378:metabolism / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007511:Ischemia / Q000188:drug therapy / Q000503:physiopathology; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008102:Liver Circulation / Q000187:drug effects; D008107:Liver Diseases / Q000188:drug therapy / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D011169:Portal Vein / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion / Q000379:methods; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000517:prevention & control; D014682:Vena Cava, Inferior / Q000502:physiology
chemical_list: D015815:Cell Adhesion Molecules; D006862:Hydrogen Sulfide; D018799:Intercellular Adhesion Molecule-1; D008054:Lipid Peroxides; D016328:NF-kappa B; C110936:Havcr1 protein, rat