Prophylactic Antiarrhythmic Effect of Anesthetics at Subanesthetic Concentration on Epinephrine-Induced Arrhythmias in Rats after Brain Death

The present study using brain death model of rats was designed to examine whether prophylactic administration of volatile anesthetics and propofol prevent the epinephrine-induced arrhythmias. A Fogarty catheter was placed intracranially for induction of brain death. After brain death, the rats were randomly assigned to five groups: the control group (no anesthetics), the sevoflurane group (0.8%), the isoflurane group (0.5%), the halothane group (0.3%), and the propofol group (195 μg·kg−1·min−1). These anesthetics were about 30% ofED50of each anesthetic. The arrhythmogenic dose of epinephrine was determined in each anesthetic group. In addition, we examined left ventricular levels of connexin 43 phosphorylation 30 min after administration of each anesthetic with Western blot analysis. The arrhythmogenic dose of epinephrine in the sevoflurane group was significantly higher than that in the control group, while the arrhythmogenic dose of epinephrine in any other anesthetic group was not different. On the other hand, the ratio of phosphorylated-connexin 43/total connexin 43 was also similar among the study groups. Thus, prophylactic administration of subanesthetic dose of sevoflurane is effective in preventing epinephrine-induced arrhythmias after brain death, but phosphorylation of connexin is not involved in the antiarrhythmic property of sevoflurane.

EFFECTS OF RESERPINE AND ADRENALINE ON ATRIAL FIBRILLATION

The resistance of isolated rabbit atria to arrhythmic factors such as low potassium medium, acetylcholine, and electrical stimulation was determined before and after contact with reserpine and following administration of large doses of adrenaline. Animals pretreated with reserpine were found more sensitive to arrhythmic factors than untreated controls. Moreover, adrenaline was shown, in most cases, to abolish the induced arrhythmias or to lower the frequency of the atrial firing rate. As already suggested by Burn, this antiarrhythmic property of adrenaline at the atrial level is considered to be the result of an antagonism with acetylcholine, presumably through a lengthening of the duration of the action potential.