title: Effects of sodium hydrosulfide on intestinal mucosal injury in a rat model of cardiac arrest and cardiopulmonary resuscitation.
abstract: OBJECTIVE
  Cardiac arrest and cardiopulmonary resuscitation (CPR) can lead to intestinal ischemia/reperfusion (I/R) injury. Increasing studies have indicated that hydrogen sulfide (H2S) is in favor of a variety of tissue I/R injury. The purpose of this study was to explore whether sodium hydrosulfide (NaHS), a H2S donor, can protect intestinal mucosa after CPR and its potential mechanisms.
  
  
  METHODS
  Male Sprague-Dawley rats were subjected to 6min cardiac arrest induced by transcutaneous electrical epicardium stimulation and then resuscitated successfully. A bolus of either NaHS (0.5mg/kg) or placebo (NaCl 0.9%) was blindly injected 1min before the start of CPR intravenously, followed by a continuous injection of NaHS (2mg/kg/h) or placebo for 3h. Intestinal and plasma samples were collected for assessments 24h after CPR.
  
  
  RESULTS
  We found that NaHS can markedly alleviate cardiac arrest induced intestinal mucosal injury. Rats treated with NaHS showed a lower malondialdehyde content, higher superoxide dismutase activity and glutathione content in intestine after CPR. Increased intestinal myeloperoxidase activity was significantly decreased by NaHS after CPR. Moreover, a reduced intestinal apoptotic cells after CPR were evident when pretreated with NaHS. Further studies indicated that NaHS enhances the expression of hypoxia-inducible factor-1α (HIF-1α) in intestine after CPR.
  
  
  CONCLUSIONS
  Our data demonstrated that NaHS treatment before CPR induces intestinal mucosal protection 24h post-resuscitation. The protective effects may be through oxidative stress reduction, inflammation alleviation, apoptosis inhibition and HIF-1α activation.
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China.
authors.forename: Hao
authors.initials: H
authors.lastname: Pan
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China.
authors.forename: Di
authors.initials: D
authors.lastname: Chen
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China.
authors.forename: Beibei
authors.initials: B
authors.lastname: Liu
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China.
authors.forename: Xuemeng
authors.initials: X
authors.lastname: Xie
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China.
authors.forename: Jincheng
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, No. 1095, Jiefang Road, Wuhan 430030, PR China. Electronic address: guangtiany@hotmail.com.
authors.forename: Guangtian
authors.initials: G
authors.lastname: Yang
mesh_terms: D061605:Administration, Intravenous; D006631:Amine Oxidase (Copper-Containing) / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D016887:Cardiopulmonary Resuscitation / Q000009:adverse effects*; D004558:Electric Stimulation; D004797:Enzyme-Linked Immunosorbent Assay; D006323:Heart Arrest / Q000150:complications*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology* / Q000517:prevention & control*; D013440:Sulfides / Q000008:administration & dosage / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D013440:Sulfides; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D006631:Amine Oxidase (Copper-Containing); C025451:sodium bisulfide