title: Effects of postconditioning of adenosine and acetylcholine on the ischemic isolated rat ventricular myocytes.
abstract: In this study, protective effects of adenosine and acetylcholine-induced postconditioning were investigated on the contractile function of the ischemic isolated rat ventricular myocytes. A video-based edge-detection system was used to monitor single ventricular myocytes contraction. Adenosine and acetylcholine were administrated for 6 min before ischemia as preconditioning, or 15 min after ischemia as postconditioning. Adenosine and acetylcholine receptor antagonists and mitoKATP inhibitor were used to analyze pathways underlying the effects on postconditioning.
  
  
  RESULTS
  (1) The peak shortening of ischemic heart cells was improved by both adenosine and acetylcholine during preconditioning (84.72+/-5.34% and 68.61+/-8.10% vs. control: 8.43+/-5.35% of the pre-ischemia value), as well as postconditioning (76.47+/-7.87% and 57.48+/-6.97% vs. control: 8.43+/-5.35% of the pre-ischemia value) and the effects of preconditioning and postconditioning were comparable. More datum in the normal text. (2) Observed effects of adenosine and acetylcholine postconditioning were missing in the presence of adenosine A1 receptor and muscarinic M2 receptor antagonists, respectively. (3) Adenosine and acetylcholine-induced postconditioning was also blocked by mitoKATP antagonist. These results suggest that both adenosine and acetylcholine protect the contractile function of ischemic heart cells to a similar extent during preconditioning and postconditioning. The postconditioning of adenosine and acetylcholine is relative to the adenosine A1 and muscarinic M2 receptors, respectively. MitoKATP is implicated in the postconditioning of both acetylcholine and adenosine.
authors.affiliation: Department of Pharmacology, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, PR China, and Research Centre, Sainte-Justine Hospital, Montreal, Canada.
authors.forename: Jun
authors.initials: J
authors.lastname: Lu
authors.forename: Wei-Jin
authors.initials: WJ
authors.lastname: Zang
authors.forename: Xiao-Jiang
authors.initials: XJ
authors.lastname: Yu
authors.forename: Bing
authors.initials: B
authors.lastname: Jia
authors.forename: Alzbeta
authors.initials: A
authors.lastname: Chorvatova
authors.forename: Lei
authors.initials: L
authors.lastname: Sun
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000241:Adenosine / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D015687:Cell Hypoxia; D048430:Cell Shape / Q000187:drug effects; D002478:Cells, Cultured; D003652:Decanoic Acids / Q000494:pharmacology; D003959:Diamines / Q000494:pharmacology; D005260:Female; D006352:Heart Ventricles / Q000166:cytology / Q000187:drug effects*; D006880:Hydroxy Acids / Q000494:pharmacology; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D015428:Myocardial Reperfusion Injury; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology; D058915:Purinergic P1 Receptor Antagonists; D051381:Rats; D017207:Rats, Sprague-Dawley; D018047:Receptors, Purinergic P1 / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology; D016276:Ventricular Function; D014970:Xanthines / Q000494:pharmacology
chemical_list: D003652:Decanoic Acids; D003959:Diamines; D006880:Hydroxy Acids; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D058915:Purinergic P1 Receptor Antagonists; D018047:Receptors, Purinergic P1; D014665:Vasodilator Agents; D014970:Xanthines; C117780:mitochondrial K(ATP) channel; C052853:5-hydroxydecanoic acid; C051360:1,3-dipropyl-8-cyclopentylxanthine; D000241:Adenosine; D000109:Acetylcholine; C054938:methoctramine