Anesthesiology
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Comparative Study
The dose-response relationship of mivacurium chloride in humans during nitrous oxide-fentanyl or nitrous oxide-enflurane anesthesia.
The dose-response relationships of mivacurium chloride during N2O/fentanyl or N2O/enflurane anesthesia were compared in 70 patients intraoperatively. Responses were defined in terms of percentage changes in the evoked twitch tension of the adductor pollicis muscle, and dose-response curves were constructed following probit transformation of the responses. End-tidal concentrations of enflurane during the were study were 0.9-1.2%. ⋯ Regression lines describing the relationship between the maximum depression of twitch tension (response) and the time interval between the injection of mivacurium and the return of twitch tension to 90% of the control value (duration) were constructed. The response-duration line for N2O/enflurane anesthesia was displaced significantly to the left of the line for N2O/fentanyl (P less than 0.05), indicating that enflurane anesthesia was associated with a prolongation of mivacurium-induced neuromuscular blockade. The neuromuscular blocking effect of mivacurium is both enhanced by and prolonged during N2O/enflurane compared with that during N2O/fentanyl anesthesia.
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This prospective clinical study evaluated the influence of high bilirubin plasma levels on the Nellcor pulse oximeter readings (SpO2). Twenty-nine icteric patients (mean total bilirubin 19.2 mg/dl, range 2.3-84.3 mg/dl) were compared with 46 controls. The difference between SpO2 and oxyhemoglobin percentage of hemoglobin (HbO2corr) or fractional saturation as measured by a seven wavelengths Corning Co 2500 Co-oximeter and corrected for the spectral error induced by hyperbilirubinemia in that co-oximeter was greater in icteric patients (bias and precision: 2.9% +/- 2.2% vs. 1.7% +/- 2.7%, P less than 0.03). ⋯ Pulse oximeters read most of CoHb as oxyhemoglobin. After correcting SpO2 for carboxyhemoglobin in both groups of patients, the 99% confidence limits from the obtained regression line were the same in icteric patients (-0.81%, 1.03%) as in controls (-0.89%, 1.08%). There was thus no demonstrable direct influence of high bilirubin plasma levels on SpO2 as measured by a Nellcor pulse oximeter.
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Hepatic uptake and distribution of nondepolarizing muscle relaxants in pigs was investigated. A portocaval shunt preparation enabled the determination of the pharmacodynamics of nondepolarizing muscle relaxants both during temporary liver exclusion and intraportal injection in the same animal. To demonstrate the validity of the model in pigs, in a pilot study the influence of hepatic uptake on neuromuscular blockade by pancuronium (n = 3) and its congener Org 6368 (n = 3) was determined. ⋯ In the pilot study the influence of hepatic uptake on neuromuscular blockade was similar for pancuronium and Org 6368. For gallamine the onset time, intensity, recovery rate, and duration of action were similar after all four injections. For Org 6368 the variables of neuromuscular blockade were similar after iv and intraportal injection, but exclusion of the liver prolonged the neuromuscular block.(ABSTRACT TRUNCATED AT 250 WORDS)
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Studies with ethanol have indicated that dihydropyridine-sensitive calcium (Ca++) channels may be involved in the adaptation to prolonged exposure to ethanol. This study investigated the effects, in mice, of the dihydropyridine Ca++ antagonist, nitrendipine, on acute tolerance to nitrous oxide after 60 min exposure to anesthetizing concentrations, and also the withdrawal syndrome which occurred following removal from nitrous oxide. Control mice were anesthetized by nitrous oxide concentrations in the range 1.28-1.51 atmospheres. ⋯ Nitrendipine diminished or prevented nitrous oxide withdrawal seizures, in a dose-dependent manner (P less than 0.05 for nitrendipine 50 and 100 mg.kg-1). These results support the importance of the role of dihydropyridine-sensitive Ca++ channels in the mechanism of tolerance and dependence to central depressant drugs. They also suggest that acute and chronic tolerance to sedative drug action may share some common pathways, and that tolerance and physical dependence may share a common mechanism through voltage-operated Ca++ channels.