The Studies on the Epinephrine - Induced Arrhythmias During Halothane Anesthesia in Dogs / 대한마취과학회지

It is known that the concurrent administration of epinephrine, whether applied subcutaneously or parenterally during halothane anesthesia, can result in the initiation of ventrieular arrhythmias, which may be life threatening. However the mechanism by which halothane sensitizes the heart to catecholamines are not known yet. The purpose of this study was to investigate the mechanism of epinephrine induced cardiac arrhythmias during 1.2 MAC halothane anesthesia in dogs. Thirty-eight dogs were randomly assigned to five groups, halothane anesthesia were measured the arrythmogenic doses of epinephrine(ADE) before and after each treatment with sodium nitroprusside (SNP) (n=9), lidocaine(n=7), propranolol(n=7), prazosin(n=7) and verapamil(n=8), and compared each other. The results were follows. 1) The control ADE to induce ventricular arrhythmias was 2.160.15 ug/kg/min. 2) Treatment with SNP resulted in a decrease(28%) in mean blood pressure, but did not increase the ADE compared to the control. 3) Lidocaine and propranolol significantly increased the control ADE by 1.5 times, respectively, but there was no different between the ADE of lidocaine and that of propranolol. 4) Prazosin and verapamil also significantly increased the control ADE by 3.3 times and 2.6 times respectively, and the increased amplitudes were significant greater than the effect noted after lidocaine or propranolol treatment. There results suggest that the mechanism of epinephrine-induced cardiac arrhythmias during halothane anesthesia is mainly mediated via alpha-1 receptor and calcium channel, and alpha-1 blocker and calcium channel blocker may be useful to prevent the epinephrine-induced cardiac arrhythmias during halothane anesthesia.

Effect of Propranolol on Serum K+ Changes Induced by Succinylcholine / 대한마취과학회지

Succinylcholine induces a small increase in serum K+ (0.3~0.5mEq/l) in normal patients, but it may produce fatal increases in sensitive conditions, including severe burn, massive trauma, tetanus and neuromuscular disorders. Recently, interest has been focussed on the role of the adrenergic system in extrarenal potassium hemeostasis. According to this concept, beta-adrenergic stimulation enhances and conversely a blockade imparis celluar uptake of potassium. Meanwhile propranolol, a beta-adrenergic blocker, is an incresingly, common drug among surgical patients. Therefore, the present experiment was carried out on 66 patients in order to determine whether propranolol augments or prolongs the increases in serum K+ following succinylcholine injection(2mg/kg, I.V.). Serum K+ and Na+ levels were measured just prior to induction and at 3,5,10,30,60,90 minutes following succinylcholine administration. The patients were divided into three groups: Group 1: 26 patients without propranolol treatment, Group 2: 20 patients pretreat with divided doses of propranolol (320 mg b.i.d. p.o.). and Group 3: 20 patients on chronic propranolol therapy. The results were as follows. 1) Baseline K+ valuses were significantly higher in propranolol treated patients(Groups 2 and 3) than in non-treated patients(Group 1). 2) The magnitude of maximum increases in serum K+ following succinylcholine was 0.19mEq/l, 0.16mEq/l and 0.21mEq/l in group 1,2 and 3, respectively. 3) The time to peak increases in K+ was 30min, 5min and 3 min following succinylcholine in group 1,2 and 3, respectively. 4) Serum Na+ decreased significantly following succinylcholine administration in all groups, but there was no significant difference among the groups at other times. These results indicate that propranolol neither augments nor prolongs increases in serum K+ following succinylcholin injection. Thus succinylcholine can be used safely in the presence of a beta-adrenergic blockade.