Anesthesiology
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Hydroxocobalamin has been shown to be a rapid and powerful antidote in acute cyanide poisoning and to prevent cyanide poisoning during sodium nitroprusside administration. However, its hemodynamic effects remain unknown. The authors therefore investigated the effects in chronically instrumented conscious dogs (n = 8) that were randomly given hydroxocobalamin (20, 70, and 140 mg.kg-1) or saline. ⋯ The largest dose (140 mg.kg-1) induced a decrease in the maximum increase of LV pressure (-7 +/- 3%; P less than 0.05), maximum aortic blood flow acceleration (-17 +/- 5%; P less than 0.05), and cardiac output (-19 +/- 6%; P less than 0.05), whereas systemic resistance increased (+41 +/- 9%; P less than 0.05). In six other dogs, local administration of hydroxocobalamin (0.5, 1.5, and 5.0 mg.kg-1.min-1) confirmed that, in large doses, this drug has direct vasoconstrictor properties affecting both conductance (decrease in iliac artery diameter: -2.5 +/- 0.8%) and resistance (decrease in iliac artery blood flow: -19.5 +/- 3.4%) vessels. Thus, hydroxocobalamin should be a safe cyanide antidote, considering the lack of hemodynamic effects within the therapeutic range of doses.
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Randomized Controlled Trial Comparative Study Clinical Trial
Desflurane and isoflurane in surgical patients: comparison of emergence time.
In order to examine the clinical potential of desflurane (difluoromethyl-1-fluoro-2,2,2-trifluoroethyl ether) in humans, a randomized, controlled study was designed to compare time of emergence from anesthesia in patients undergoing elective surgery under desflurane anesthesia to that of patients under isoflurane anesthesia. Twenty-eight patients were randomly divided into four groups. Group 1 received isoflurane 0.65 MAC; group 2, desflurane 0.65 MAC; group 3, isoflurane 1.25 MAC; and group 4, desflurane 1.25 MAC. ⋯ Patients receiving isoflurane 0.65 MAC responded to commands 15.6 +/- 4.3 min after discontinuation of the anesthetic; patients in the desflurane 0.65 MAC group responded in 8.8 +/- 2.7 min (P less than 0.01). Emergence time for isoflurane 1.25 MAC was 30.0 +/- 11.0 min; for desflurane 1.25 MAC it was 16.1 +/- 6.0 min (P less than 0.05). Our results confirm that emergence from desflurane anesthesia is more rapid than from isoflurane.
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Randomized Controlled Trial Clinical Trial
Effects of residual concentrations of isoflurane on the reversal of vecuronium-induced neuromuscular blockade.
Thirty-six anesthetized patients (ASA physical status 1 or 2) undergoing elective surgery were monitored (isometric adductor pollicis mechanical activity) to detect the effects of discontinuing isoflurane anesthesia upon the reversal of vecuronium-induced neuromuscular blockade. Neuromuscular blockade was produced by vecuronium 100 micrograms/kg and additional doses of 20 micrograms/kg until completion of surgery. The patients were randomly divided into three groups: in the control group (n = 12), only fentanyl/N2O was given; in the "isostable" group (n = 12), isoflurane at an end-tidal concentration of 1.25% was maintained throughout anesthesia; in the "isostop" group (n = 12), isoflurane 1.25% was discontinued before neostigmine administration. ⋯ In the isostable group, final mean train-of-four was significantly less (75%) than in the other patients (88%) (P less than 0.01). Mean tetanic fade at 100 Hz was significantly less in the isostable group (31%) than in the isostop group (57%) (P less than 0.01) and control group (84%) (P less than 0.01). We conclude that discontinuing isoflurane anesthesia for 15 min improves the reversal of a vecuronium paralysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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Comparative Study
Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog.
The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. ⋯ In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.