ROLE OF THE VAGUS NERVE IN THE ANTIDYSRHYTHMIC EFFECT OF DEXMEDETOMIDINE ON HALOTHANE EPINEPHRINE DYSRHYTHMIAS IN DOGS/

Citation
T. Kamibayashi et al., ROLE OF THE VAGUS NERVE IN THE ANTIDYSRHYTHMIC EFFECT OF DEXMEDETOMIDINE ON HALOTHANE EPINEPHRINE DYSRHYTHMIAS IN DOGS/, Anesthesiology, 83(5), 1995, pp. 992-999
Citations number
42
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
83
Issue
5
Year of publication
1995
Pages
992 - 999
Database
ISI
SICI code
0003-3022(1995)83:5<992:ROTVNI>2.0.ZU;2-Q
Abstract
Background: Dexmedetomidine, an alpha(2)-adrenergic agonist, can preve nt the genesis of halothane/epinephrine dysrhythmias through the centr al nervous system, Because stimulation of alpha(2) adrenoceptors in th e central nervous system enhances vagal neural activity and vagal stim ulation is known to inhibit digitalis-induced dysrhythmias, dexmedetom idine may exert the antidysrhythmic property through vagal stimulation , To address this hypothesis, the effect of dexmedetomidine in vagotom ized dogs was examined and compared with that in intact dogs. in addit ion, the effect of vagotomy on the antidysrhythmic action of doxazosin , an alpha(1) antagonist, was studied. Methods: Adult mongrel dogs wer e anesthetized with halothane (1.3%) and monitored continuously for sy stemic arterial pressure and premature ventricular contractions. Anima ls were divided into two groups receiving bilateral vagotomy or sham o peration. The dysrhythmia threshold was expressed by the dysrhythmogen ic dose of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, and pla sma concentration of epinephrine at the time when the dysrhythmogenic dose was reached. The threshold was determined in the presence of dexm edetomidine (a selective alpha(2) agonist that crosses the blood-brain barrier) and doxazosin (a selective a, antagonist that does not penet rate the blood-brain barrier) in the two groups. In addition, the effe ct of dexmedetomidine in the presence of atropine methylnitrate instea d of vagotomy was examined, Results: Vagotomy did not affect the basal vulnerability to halothane/epinephrine dysrhythmias significantly, Al though dexmedetomidine dose-dependently prevented the genesis of the d ysrhythmias in intact dogs, the beneficial effect of dexmedetomidine w as abolished in both the vagotomized and the atropine-treated dogs. On the other hand, vagotomy did not change the antidysrhythmic property of doxazosin, Conclusions: The vagus nerve plays an important role in the prevention of halothane/epinephrine dysrhythmias by dexmedetomidin e in dogs, However, resting vagal tone neither modulates the onset of halothane/epinephrine dysrhythmias nor affects the antidysrhythmic act ion of doxazosin.