title: PI3K-Akt/eNOS in remote postconditioning induced by brief pulmonary ischemia.
abstract: OBJECTIVE
  Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model.
  
  
  METHODS
  Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined.
  
  
  RESULTS
  Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2.
  
  
  CONCLUSIONS
  Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.
authors: . tyh6565@163.com.
authors: Yan-hua
authors: YH
authors: Tang
authors: Jue-shen
authors: JS
authors: Yang
authors: Hai-yan
authors: HY
authors: Xiang
authors: Jia-jun
authors: JJ
authors: Xu
mesh_terms: D000818:Animals; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D019194:Ischemic Preconditioning / Q000379:methods*; D008168:Lung / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D011817:Rabbits; D013482:Superoxide Dismutase / Q000097:blood; D054460:rho-Associated Kinases / Q000378:metabolism
chemical_list: D008315:Malondialdehyde; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D054460:rho-Associated Kinases; D003402:Creatine Kinase; D019331:NG-Nitroarginine Methyl Ester