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
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.