Anesthesiology
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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.
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Recovery from anesthesia was assessed in a controlled manner in 34 healthy student volunteers, using a psychomotor test battery 1 and 5 hours and a driving simulator 2, 4.5, and 7 hours after 3.5 minutes of anesthesia with halothane or enflurane combined with nitrous oxide and oxygen. Psychomotor performances remained significantly (P less than 0.05 to P less than 0.001) worse than in an unanesthetized control group for 5 hours after both halothane and enflurane. ⋯ It is concluded that after even brief periods of halothane or enflurane anesthesia patients should not drive or operate machinery for at least 7 hours. The magnitudes and durations of the residual effects of both agents on psychomotor performance were, however, less than those previously found after thiopental, methohexital, or diazepam.
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In dogs anesthetized with pentobarbital-chloralose, cardiac output and blood flows of four regional vascular beds (superior mesenteric, left renal, left circumflex coronary and left femoral) were continuously monitered with electromagnetic flowmeters. Arterial blood pressure and heart rate were also measured. Hypotension was induced with intravenous infusions of sodium nitroprusside and trimethaphan for 5-16 min to produce comparable reductions of mean arterial pressure (32 mm Hg or 26 per cent with nitroprusside and 37 mm Hg or 31 per cent with trimethaphan). ⋯ Nitroprusside affected femoral blood flow minimally, with a slight reduction of femoral vascular resistance. In contrast, trimethaphan increased femoral blood flow and markedly decreased femoral vascular resistance. Redistribution of cardiac output favoring the dilated skin and muscle vascular beds appears to be an important undesirable effect of trimethaphan.