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Because the relative efficacy of antiarrhythmic agents on halothane-epinephrine arrhythmias has not been well characterized, this study was undertaken to comparatively evaluate the antiarrhythmic action of Na(+)-, K(+)- and Ca(2+)-channel blockers on epinephrine-induced ventricular arrhythmias during halothane anesthesia in rats.Rats were anesthetized at random with either halothane (1.5%), isoflurane (2.0%), or pentobarbital (50 mg/kg intraperitoneally), and the lungs were mechanically ventilated with oxygen. The rats were studied in three consecutive protocols. Protocol I determined the arrhythmogenic thresholds of epinephrine during the three types of anesthesia in 33 rats. Protocol II determined the arrhythmogenic thresholds of epinephrine during halothane anesthesia in 64 rats receiving saline (control) or one of five antiarrhythmic agents. Protocol III measured the duration of epinephrine-induced arrhythmias during halothane anesthesia in 42 rats receiving saline (control) or one of five antiarrhythmic agents.In protocol I, the arrhythmogenic doses of epinephrine during halothane, isoflurane, or pentobarbital anesthesia were 1.7 +/- 3.2, 11.1 +/- 0.6, and 39.0 +/- 3.9 micrograms/kg, respectively, and the corresponding plasma concentrations were 4.3 +/- 0.8, 103.7 +/- 9.2, and 246.7 +/- 28.9 ng/ml, respectively. In protocol II, the arrhythmogenic doses were similar in rats receiving saline and in those receiving lidocaine. The arrhythmogenic doses in rats receiving verapamil, flecainide (Na(+)- and K(+)-channel blocker), E-4031 (K(+)-channel blocker), or amiodarone(K(+)-channel blocker with Na(+)-, Ca(2+)-, and beta-blocking activity) increased significantly, i.e., 4.2, 4.2, 5.5, and 31.7 times control (P0.01). In protocol III, lidocaine had no effect on the duration of arrhythmias. Flecainide, E-4031, and verapamil markedly reduced the duration of arrhythmias induced by epinephrine, 8 micrograms/kg intravenously (P0.01), whereas only amiodarone markedly reduced the duration of arrhythmias induced by epinephrine, 16 micrograms/kg intravenously (P0.01).It was concluded that agents with K(+)-channel blocking properties were the most effective in preventing halothane-epinephrine arrhythmias in rats.

This study was carried out to determine the relative potencies of local anaesthetics to inhibit the cholinergic synaptic transmission using cultured bovine adrenal chromaffin cells, and to clarify if the inhibitory action would correlate with biophysical and pharmacological properties. Local anaesthetics (bupivacaine, etidocaine, tetracaine, lignocaine and procaine; 0·02–2 Mm) inhibited carbachol-induced catecholamine release from the cells in a concentration-dependent manner. This inhibition was completely reversible. IC50 (concentration of 50% inhibition) of each anaesthetic showed no correlation with the lipid solubility. The local anaesthetics showed greater inhibitory potency at a higher extracellular pH. The results suggest that clinically relevant concentrations of local anaesthetics inhibit the stimulus-secretion coupling in the chromaffin cells. The un-ionized base form plays a major role, and the inhibitory potency does not depend on the lipid solubility of the anaesthetics.

食道癌根治術後の呼吸管理中に気道潰瘍からの持続的出血と気管壁からの大量のエアーリークをきたした症例を経験した.これは縦隔リンパ節郭清や気管周囲組織の剥離により気管の脆弱化,血流低下のために潰瘍形成や気管穿孔を起こしたためと考えられた.この症例に対して左右分岐型ダブルルーメン気管切開チューブ(DLTT)を用いることにより血液垂れ込みの防止,損傷部の安静が可能となりウィーニングに成功した.気管壁に損傷がある症例には両気管支のカフでブロックし損傷部の安静をはかる必要がある.このような場合,気管分岐部から左右上葉気管支までの距離を測定し両気管支のカフでブロックできるようなチューブを作製するのがよい.

This study was designed to analyze quantitatively the interaction of nicardipine with vecuronium using a constant infusion technique. Forty-seven patients undergoing elective otolaryngeal surgery were anesthetized with isoflurane (1% end-tidal) and nitrous oxide (67%). Patients were randomly assigned to receive one of four doses of nicardipine (0, 1, 2, and 3 micrograms.kg-1.min-1). Vecuronium infusion dose requirement was determined as a constant infusion rate which maintained 90% depression of control twitch tension. Nicardipine significantly decreased the vecuronium requirement in a dose-dependent manner, i.e., the vecuronium doses were 0.70 +/- 0.03, 0.55 +/- 0.04, 0.42 +/- 0.04, and 0.37 +/- 0.05 micrograms.kg-1.min-1 at nicardipine doses of 0, 1, 2, and 3 micrograms.kg-1.min-1, respectively. Nicardipine also reduced both the plasma concentration of vecuronium to maintain the 90% depression and the total plasma clearance of vecuronium. The reversal of the vecuronium effect with neostigmine was not influenced by nicardipine. The results indicate that the vecuronium infusion dose requirements are reduced as much as 53% by a clinical dose of nicardipine.

Although propofol is a widely used intravenous anesthetic, its effect on epinephrine-induced arrhythmias remains unknown. This study examined the possible interaction between propofol and epinephrine that might affect the induction of ventricular arrhythmias in dogs. The arrhythmogenic threshold of epinephrine was determined during anesthesia with halothane alone, propofol alone, etomidate alone, or etomidate plus varying doses of propofol. The arrhythmogenic dose and the corresponding plasma concentration of epinephrine during propofol anesthesia (blood propofol concentration 18.0 +/- 0.98 micrograms/ml) were 2.52 +/- 0.43 micrograms.kg-1.min-1 and 23.6 +/- 8.5 ng/ml, respectively. During halothane anesthesia (end-tidal 1.3 MAC), they were 2.66 +/- 0.21 micrograms.kg-1.min-1 and 35.7 +/- 1.9 ng/ml, respectively. During etomidate anesthesia, they were 9.67 +/- 1.06 micrograms.kg-1.min-1 and 205 +/- 27.5 ng/ml, respectively. The dose-effect relationship for propofol was examined during etomidate plus propofol anesthesia. Propofol reduced the arrhythmogenic plasma concentration of epinephrine in a concentration-dependent manner: at blood propofol concentrations of 2.33 +/- 0.46, 5.46 +/- 0.71, and 11.2 +/- 0.81 micrograms/ml, the corresponding plasma epinephrine concentrations were 182.6 +/- 52.5, 89.0 +/- 28.8, and 26.6 +/- 6.9 ng/ml, respectively. These results suggest that propofol enhances epinephrine-induced arrhythmias in a dose-dependent manner in dogs.