title: Intestinal ischemia preconditions myocardium: role of protein kinase C and mitochondrial K(ATP) channel.
abstract: OBJECTIVE
  The present study was designed to test the hypothesis that intestinal ischemia results in an early preconditioning against myocardial infarction and that the mechanism of the early preconditioning involves the activation of protein kinase C-mitochondrial K(ATP) channel signaling pathway in anesthetized rats.
  
  
  METHODS
  Rats were either preconditioned with a 25-min occlusion of the superior mesenteric artery followed by 15 min of reperfusion or underwent a 40-min sham period. Subsequently, all rats were subjected to a sustained 30 min of coronary occlusion and 180 min of reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining.
  
  
  RESULTS
  In sham-operated rats receiving no pharmacological intervention, the percentage of myocardial infarct within the area at risk and left ventricle was 73+/-4% and 31+/-2%, respectively, and these were significantly reduced to 44+/-4% and 23+/-1% (P<0.01) after intestinal ischemia preconditioning. Intravenous injection of protein kinase C inhibitors chelerythrine (5 mg/kg) and staurosporine (50 microg/kg) or a specific mitochondrial K(ATP) channel inhibitor 5-hydroxydecanoate (5 mg/kg) 5 min before sustained myocardial ischemia abolished the preconditioning afforded by intestinal ischemia. However, hexamethonium, a ganglion blocker, did not attenuate the preconditioning.
  
  
  CONCLUSIONS
  These data provide pharmacological evidence that protein kinase C and mitochondrial K(ATP) channel are involved in the mechanism of the early preconditioning induced by intestinal ischemia.
authors.affiliation: First Department of Surgery, Kagawa Medical University, 1750-1, Ikenobe, Miki, Kita, Japan. wang@kms.ac.jp
authors.forename: You-Ping
authors.initials: YP
authors.lastname: Wang
authors.forename: Hajime
authors.initials: H
authors.lastname: Maeta
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Mizoguchi
authors.forename: Takeo
authors.initials: T
authors.lastname: Suzuki
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Yamashita
authors.forename: Masahiro
authors.initials: M
authors.lastname: Oe
mesh_terms: D000470:Alkaloids; D000704:Analysis of Variance; D000818:Animals; D053119:Benzophenanthridines; D001794:Blood Pressure; D003652:Decanoic Acids / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006880:Hydroxy Acids / Q000494:pharmacology; D007422:Intestines / Q000098:blood supply*; D019194:Ischemic Preconditioning / Q000379:methods*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D023421:Models, Animal; D017202:Myocardial Ischemia / Q000378:metabolism; D010617:Phenanthridines / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D019311:Staurosporine / Q000494:pharmacology; D013997:Time Factors
chemical_list: D000470:Alkaloids; D053119:Benzophenanthridines; D003652:Decanoic Acids; D004791:Enzyme Inhibitors; D006880:Hydroxy Acids; D010617:Phenanthridines; D026902:Potassium Channel Blockers; D015221:Potassium Channels; C052853:5-hydroxydecanoic acid; C016299:chelerythrine; D011493:Protein Kinase C; D019311:Staurosporine