title: Role of adenosine receptors in late preconditioning against myocardial stunning in conscious rabbits.
abstract: Conscious rabbits underwent six 4-min coronary occlusions interspersed with 4-min periods of reperfusion for 2 consecutive days (days 1 and 2 of stage I); 2 wk later, they underwent the same protocol (days 1 and 2 of stage II) except that they received either 8-(p-sulfophenyl)theophylline (SPT) on day 1 (group I, n = 5) or 2-chloro-N6-cyclopentyl-adenosine (CCPA) on the day before day 1 (group II, n = 6). In both groups I and II, on day 1 of stage I, systolic wall thickening (WTh) remained significantly depressed for several hours, indicating myocardial stunning; on day 2, however, the total deficit of WTh was approximately 50% less than on day 1 (P < 0.01), indicating the development of late preconditioning (PC) against myocardial stunning. Despite administration of SPT, in group I the deficit of WTh during stage II was 55% less on day 2 than on day 1 (P < 0.05). Similar results were obtained in three other rabbits treated with PD-115199 on day 1. In group II, pretreatment with CCPA during stage II failed to decrease the deficit of WTh on day 1. This study presents a new conscious rabbit model for studying myocardial stunning that is relatively inexpensive and technically less demanding than larger animal models. In this model, the development of late PC against myocardial stunning is not blocked by nonselective blockade of adenosine receptors with either SPT or PD-115199, nor is it induced by activation of adenosine A1 receptors with CCPA, indicating that adenosine receptors are not involved in the pathogenesis of this phenomenon.
authors.affiliation: Experimental Research Laboratory, University of Louisville, Kentucky 40292, USA.
authors.forename: C
authors.initials: C
authors.lastname: Maldonado
authors.forename: Y
authors.initials: Y
authors.lastname: Qiu
authors.forename: X L
authors.initials: XL
authors.lastname: Tang
authors.forename: M V
authors.initials: MV
authors.lastname: Cohen
authors.forename: J
authors.initials: J
authors.lastname: Auchampach
authors.forename: R
authors.initials: R
authors.lastname: Bolli
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004562:Electrocardiography; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D015425:Myocardial Reperfusion; D017682:Myocardial Stunning / Q000503:physiopathology / Q000517:prevention & control*; D058915:Purinergic P1 Receptor Antagonists; D011687:Purines / Q000494:pharmacology; D011817:Rabbits; D018047:Receptors, Purinergic P1 / Q000502:physiology*; D013449:Sulfonamides / Q000494:pharmacology; D013599:Systole; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D016277:Ventricular Function, Left; D000096926:Benzenesulfonamides
chemical_list: D058915:Purinergic P1 Receptor Antagonists; D011687:Purines; D018047:Receptors, Purinergic P1; D013449:Sulfonamides; D013806:Theophylline; C052023:N-(2-(dimethylamino)ethyl)-N-methyl-4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)benzenesulfonamide; D000096926:Benzenesulfonamides; C031433:8-(4-sulfophenyl)theophylline