title: Suppression of reperfusion arrhythmia by ischemic preconditioning in the rat: is it mediated by the adenosine receptor, prostaglandin, or bradykinin receptor?
abstract: The mechanism for the suppression of reperfusion arrhythmia by preconditioning (PC) remains unknown. This study aimed to examine the roles of the adenosine receptor, prostaglandin (PG), and bradykinin (BK) receptor in PC. Under pentobarbital anesthesia, the coronary artery of the rat was occluded for 5 min and then reperfused. In untreated controls, this protocol induced ventricular tachycardia (VT) in 100% of the rats and ventricular fibrillation (VF) in 60%. PC with 2 min ischemia/5 min reperfusion prior to the 5 min coronary occlusion significantly reduced the incidence of reperfusion VT and VF to 30% and 0%, respectively. This antiarrhythmic effect of the PC was not blocked when rats were pretreated with 8-phenyltheophylline (8-PT, 10 mg/kg), aspirin-DL-lysin (18 mg/kg), or a specific BK receptor antagonist, Hoe140 (20 nmol/kg). None of these agents alone significantly modified the incidence of reperfusion VT or VF. These results suggest that neither the adenosine receptor, endogenous PG, nor BK receptor play a major role in the mechanism of suppression of perfusion arrhythmias by PC in the rat heart.
authors.affiliation: Second Department of Internal Medicine, Sapporo Medical University, School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Miura
authors.forename: R
authors.initials: R
authors.lastname: Ishimoto
authors.forename: J
authors.initials: J
authors.lastname: Sakamoto
authors.forename: A
authors.initials: A
authors.lastname: Tsuchida
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: K
authors.initials: K
authors.lastname: Shimamoto
authors.forename: O
authors.initials: O
authors.lastname: Iimura
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000517:prevention & control*; D001241:Aspirin / Q000031:analogs & derivatives / Q000494:pharmacology; D001920:Bradykinin / Q000031:analogs & derivatives / Q000494:pharmacology; D065168:Bradykinin Receptor Antagonists; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D008239:Lysine / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018002:Receptors, Bradykinin / Q000502:physiology*; D018047:Receptors, Purinergic P1 / Q000502:physiology*; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000319:Adrenergic beta-Antagonists; D000894:Anti-Inflammatory Agents, Non-Steroidal; D065168:Bradykinin Receptor Antagonists; D011453:Prostaglandins; D018002:Receptors, Bradykinin; D018047:Receptors, Purinergic P1; C065679:icatibant; D013806:Theophylline; C028322:8-phenyltheophylline; D008239:Lysine; D001241:Aspirin; D001920:Bradykinin; C010395:acetylsalicylic acid lysinate