title: [The role of nitric oxide in ethanol postconditioning induced cardioprotection].
abstract: OBJECTIVE
  To investigate whether the release of nitric oxide (NO) was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts.
  
  
  METHODS
  Hearts isolated from male SD rats were subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min (at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min). The rats were divided into five groups: normal, ischemia and reperfusion, ethanol postconditioning, ethanol postconditioning + L-nitro-arginine-methylester (L-NAME) and ethanol postconditioning + atractyloside. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis.
  
  
  RESULTS
  In contrast to ischemia and reperfusion, ethanol postconditioning improved left ventricular developed pressure, rate pressure product during reperfusion, reduced LDH release and infarct size. NO content was decreased. The ratio of Bcl-2/Bax was increased. Administration of nitric oxide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning, which inhibited the recovery of hemodynamic parameters, the decreases of LDH and infarct size. NO content was decreased further. The ratio of Bcl-2/Bax was decreased.
  
  
  CONCLUSIONS
  The cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release, inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.
authors.affiliation: Department of Physiology, Bengbu Medical College, Bengbu 233030, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Hu
authors.forename: Ying
authors.initials: Y
authors.lastname: Yu
authors.forename: Cui-Rong
authors.initials: CR
authors.lastname: Jiang
authors.forename: Su-Dong
authors.initials: SD
authors.lastname: Guan
authors.forename: Zheng-Hong
authors.initials: ZH
authors.lastname: Li
mesh_terms: D000818:Animals; D000431:Ethanol / Q000627:therapeutic use*; D066298:In Vitro Techniques; D057775:Ischemic Postconditioning; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D009569:Nitric Oxide; D000431:Ethanol