Anesthesiology
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The relative central nervous system and cardiovascular toxicity of bupivacaine was compared in pregnant and nonpregnant ewes during continuous infusion of bupivacaine into the jugular vein at the rate of 0.5 mg X kg-1 X min-1. In all animals, identical symptoms of toxicity occurred in the following order: convulsions, hypotension, respiratory arrest, and circulatory collapse. The dose of bupivacaine required to produce central nervous system (CNS) toxicity in the pregnant ewe tended to be lower than in the nonpregnant animal, although the difference was not statistically significant (P less than 0.1). ⋯ Similarly, bupivacaine blood concentrations at the onset of respiratory arrest and circulatory collapse were lower in the pregnant group, being 5.2 +/- 0.7 micrograms/ml and 5.5 +/- 0.8 micrograms/ml, respectively, versus 7.5 +/- 1.0 microgram/ml and 8.0 +/- 0.9 micrograms/ml, respectively, in the nonpregnant group (P less than 0.05). The concentration of bupivacaine in the brain of pregnant ewes at the time of cardiovascular collapse was significantly lower (P less than 0.01) than in the nonpregnant group (7.5 +/- 1.5 vs. 16.3 +/- 1.7 micrograms/g). The myocardial tissue concentration of bupivacaine also tended to be lower in the pregnant group, although the differences were not statistically significant (P less than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)
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This study examines in vitro the contractures induced by halothane and succinylcholine in skeletal muscle taken as biopsy specimens from 42 patients referred to the authors' laboratory for diagnosis of malignant hyperthermia (MH) susceptibility. In addition, possible differences between the response of preparations from these same patients with and without a history of masseter muscle rigidity following succinylcholine (SCh) administration were determined to investigate the in vitro relationship of masseter muscle rigidity to MH. Halothane 3%-induced contractures in preparations from MH susceptibles were similar, whether the group had a history of masseter muscle rigidity (1.15 +/- 0.18 g; n = 10) or not (1.02 +/- 0.21 g; n = 14). ⋯ In contrast, halothane added in the presence of SCh did not induce contractures to the same extent in preparations from MH-negative patients without a history of masseter muscle rigidity. This is the first reported in vitro method by which to examine the clinically troublesome interaction between SCh and halothane. This approach also may prove to be important in further investigations of the relationship between masseter muscle rigidity and MH.
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The authors obtained boiling point-composition data and vapor pressure-composition data for the halothane-enflurane system at 20 degrees C and 25 degrees C. This was used to demonstrate the existence of an azeotropic mixture of halothane and enflurane and to predict the output of an enflurane vaporizer contaminated with different amounts of halothane and a halothane vaporizer contaminated with different amounts of enflurane. ⋯ It was concluded that when halothane and enflurane vaporizers are mounted in series, the halothane should be downstream. It is explained why the halothane-enflurane azeotrope is unlikely to be useful clinically.