ADRENOCEPTOR MECHANISM INVOLVED IN THIOPENTAL-INDUCED POTENTIATION OFHALOTHANE-EPINEPHRINE ARRHYTHMIAS IN DOGS

Citation
T. Kamibayashi et al., ADRENOCEPTOR MECHANISM INVOLVED IN THIOPENTAL-INDUCED POTENTIATION OFHALOTHANE-EPINEPHRINE ARRHYTHMIAS IN DOGS, Research communications in molecular pathology and pharmacology, 93(2), 1996, pp. 225-234
Citations number
17
Categorie Soggetti
Pharmacology & Pharmacy",Pathology,Biology
ISSN journal
10780297
Volume
93
Issue
2
Year of publication
1996
Pages
225 - 234
Database
ISI
SICI code
1078-0297(1996)93:2<225:AMIITP>2.0.ZU;2-F
Abstract
Although thiopental is known to potentiate halothane-epinephrine arrhy thmias, the precise mechanism of this potentiation is obscure. The aut hors investigated the comparative role of alpha(1) and beta adrenergic actions in the thiopental-induced potentiation of halothane-epinephri ne arrhythmias in dogs. Adult mongrel dogs were anesthetized with halo thane alone (1.3%) or thiopental (20 mgkg(-1)) plus halothane and moni tored continuously for systemic arterial pressures and for premature v entricular contractions. The arrhythmogenic doses of phenylephrine and isoproterenol were determined during the two anesthetic methods and t he effect of thiopental on the arrhythmogenic action of alpha(1) and b eta agonists was examined. Thiopental failed to exert a significant po tentiation of arrhythmogenic effect of phenylephrine or isoproterenol, when these agents were administered separately. On the other hand, th e potentiation of arrhythmogenicity by thiopental was remarkable in th e case of combined administration of both the agonists, that is, thiop ental enhanced the synergistic interaction between phenylephrine and i soproterenol for inducing arrhythmias during halothane anesthesia. In addition, the potentiation was more prominent when a low dose of isopr oterenol and a high dose of phenylephrine was combined than that when a high dose of isoproterenol and a low dose of phenylephrine was given in combination. The results indicate that thiopental significantly po tentiates the arrhythmogenic interaction of alpha(1) and beta adrenerg ic agonists administered concurrently, although individual potentiatio n of these agonists is not significant.