Anesthesiology
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To determine the effects of variations in temperature on the neuromuscular blockade produced by pancuronium, the drug was infused intravenously into 18 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch tension of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean (+/-SE) infusion rates of pancuronium needed were 0.44 +/- 0.05, 0.99 +/- 0.11, and 1.05 +/- 0.09 microng/kg/min (r = 0.73) at 29, 37, and 41 C, respectively. ⋯ The durations of neostigmine action were longer at 29 and 37 than at 41 C. It is concluded that hypothermia augments neuromuscular blockade produced by pancuronium and prolongs the time to peak effect, and possibly the duration of action, but not the dose of neostigmine needed to antagonize the blockade.
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Disordering, fluidizing and dilating effects of anesthetics upon cell membranes are well recognized. The fluidization can be precisely measured with phospholipid membranes. When phospholipids are dispersed in water, they form globules of bilayer structure. ⋯ The normalized values of the fluidizing action of these drugs at physiologic conditions correlated well with their nerve-blocking potencies. The present results indicate that the uncharged molecules fluidize the lecithin membrane by unsaturable nonspecific binding. The possible effect of the charged molecules upon the fluidity of natural membranes remains to be established.
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The purpose of this study was to examine the effects of pharmacologic alterations of adrenergic terminating mechanisms by cocaine, tropolone, aminophylline, and ketamine on the ability of epinephrine to induce arrhythmias during halothane-nitrous oxide anesthesia in dogs. Because the first three drugs inhibit intraneuronal uptake of catecholamines, extraneuronal catechol-O-methyl transferase (COMT), and phosphodiesterase, respectively, they might be expected to potentiate epinephrine-induced arrhythmias. To evaluate this possibility, the authors devised a technique for determining the minimal arrhythmic dosage of epinephrine that permitted graded assessment of changes in the sensitivity of the heart to epinephrine-induced arrhythmias. ⋯ Ketamine, according to several investigators, also appears to block reuptake of catecholamines, and when studied was also found to enhance the arrhythmogenicity of epinephrine. The extent of enhancement was comparable to that seen with cocaine. These results indicate that drugs like cocaine and ketamine that interfere with intraneuronal uptake can facilitate the development of epinephrine-induced arrhythmias and that the successive pharmacologic interference of intraneuron uptake, COMT, and phosphodiesterase leads to a stepwise increase in the arrhythmogenicity of epinephrine.
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Various amounts of carbon dioxide were removed through an extracorporeal membrane lung in spontaneously breathing lambs. The decrease in alveolar ventilation was proportional to the fraction of total carbon dioxide removed by the membrane lung. When extracorporeal CO2 removal approximated CO2 production (VCO2), alveolar ventilation almost ceased. Pulmonary ventilation can be controlled by extracorporeal carbon dioxide removal.