ACTION OF ADENINE-DERIVATIVES ON EXPERIMENTAL ATRIAL-FLUTTER IN THE CANINE HEART

Citation
Jl. Alvarado et G. Pastelin, ACTION OF ADENINE-DERIVATIVES ON EXPERIMENTAL ATRIAL-FLUTTER IN THE CANINE HEART, Archives of medical research, 28(3), 1997, pp. 329-335
Citations number
37
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
01884409
Volume
28
Issue
3
Year of publication
1997
Pages
329 - 335
Database
ISI
SICI code
0188-4409(1997)28:3<329:AOAOEA>2.0.ZU;2-A
Abstract
We have studied the effects of adenosine (Ado) and adenosine derivativ es on an experimental atrial flutter (AFL) in the canine heart. Moreov er, we have assessed these adenine derivatives on some electrophysiolo gical parameters (the conduction time and functional refractory period ) of the posterior internodal pathway (PIP) and of the ordinary atrial myocardium (OAM). The adenosine derivatives assessed were adenosine 5 '-monophosphate (AMP), adenosine 3' 5'-monophosphate (cAMP) and adenos ine 5'-triphosphate (ATP). Ado, AMP, and cAMP transformed the atrial f lutter into a short episode of atrial fibrillation that terminated spo ntaneously to sinus rhythm. This effect was prevented by previous bloc kade of A(1) purinergic receptors with aminophylline, but not by paras ympathectomy (vagotomy and atropine). ATP also suppressed the AFL, but in this case, sinus rhythm was achieved without an intermediate episo de of atrial fibrillation, and the effect of ATP was not prevented by A(1) purinergic blockade. Ado, AMP and cAMP extended the functional re fractory period measured in the PIP, but reduced this parameter in the OAM (p < 0.01). The different response of atrial tissues to the adeno sine and its monophosphate derivatives was not elicited by ATP. This d erivative caused a prolongation of FRP on both atrial tissues PIP and OAM (p < 0.05). The changes produced by Ado and its monophosphate deri vatives on FRP was blocked by aminophylline. The effect of adenine der ivatives on AFL may be explained by the dispersion of refractoriness t reated as a result of the heterogeneous response of atrial tissues to these agents. Our results support the hypothesis of an agonistic actio n of adenine derivatives on atrial purinergic receptors.