Anaesthetics and porphyria.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E S Munson.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Arterial plasma lidocaine concentration of 1 to 3.5 microgram/ml produced dose-related decreases in enflurane requirement (MAC) ranging from 15 to 37 per cent in dogs. The ventilatory responses to carbon dioxide at comparable depths of anesthesia with enflurane alone and the enflurane-lidocaine combination were measured in each animal and compared. With both anesthetic regimens there were increases in resting arterial carbon dioxide tension (mean maximal increase = 18 torr) and a 69 per cent decrease in the slope of the ventilatory response as depth of anesthesia increased. The effect of the drug interaction appears to be additive, since the ventilatory depression produced by the enflurane-lidocaine combination was no greater than that produced by enflurane alone at equivalent levels of anesthesia.
The minimum alveolar concentration (MAC) of aliflurane was measured in ten dogs. A value of 1.84 volumes per cent was determined, which correlates well with predictions based on lipid solubility. Induction of anesthesia and recovery were rapid, as would be anticipated with an agent of relatively low solubility in blood (blood-gas partition coefficient = 1.7). Circulatory responses over a relatively narrow range of aliflurane concentrations (0.8 to 1.4 MAC) remained stable, but the development of tachypnea, irregular ventilatory patterns, and increased muscle tone were frequently encountered during aliflurane anesthesis.
The effects of lidocaine and its primary metabolite monoethylglycinexylidide (MEGX) on isolated human muscle strips from non-gravid and gravid uteri were evaluated. No differences between the effects of lidocaine and those of MEGX on gravid and non-gravid muscle strips were observed. Lidocaine produced significant (P less than 0.01) dose-related depression of uterine contractility, although significant pharamacologic depression occurred only at lidocaine concentrations in excess of 25 microgram/ml. MEGX produced no consistent changes in any of the responses measured.
The relationship between infusion rate of etidocaine and bupivacaine and central nervous system toxicity was studied in three rhesus monkeys. Increasing the infusion rate from 0.5 to 2.0 mg/kg.min-1 decreased the seizure dosage of etidocaine but had no effect on that of bupivacaine. Arterial plasma concentrations of etidocaine and bupivacaine that induced electrical seizure activity increased as the infusion rate was increased from 0.5 to 1.0 mg/kg. min-1. A plasma decay study in a fourth animal demonstrated that etidocaine decayed more rapidly than did bupivacaine. These results suggest that the rate of administration of these agents is important in determining central nervous system toxicity.
The effects of equipotent concentrations of enflurane, isoflurane, and halothane on isolated human uterine muscle have been evaluated. Three anesthetic concentrations (0.5, 1.9, and 1.5 MAC) were studied. Specimens included myometrial strips from 45 non-gravid and seven gravid uteri. Both groups of muscle strips showed significant (P less than 0.05) and progressive depression of contractility with all anesthetics. However, the extents of depression at each anesthetic level studied were similar with all drugs. Enflurane, isoflurane, and halothane are equally depressing to isolated human uterine muscle.
The central-nervous-system toxicities of local anesthetic mixtures consisting of lidocaine and etidocaine or lidocaine and tetracaine, administered intravenously to four healthy, non-medicated rhesus monkeys, were evaluated. Toxicities were compared by determining seizure dosages for each drug alone and then in a lidocaine-etidocaine-tetracaine mixture. Arterial plasma levels of lidocaine and etidocaine at which electrical seizure activity occurred also were measured when the drugs were administered alone and in combination. The seizure dosages and arterial plasma levels for the drug mixtures studied were equal to the sums of the dosages and thresholds for individual constituents of the mixtures. Under the conditions of this investigation local anesthetic toxicity was additive. (Key words: Anesthetics, local, lidocaine; Anesthetics, local, etidocaine; Anesthetics, local, tetracaine; Brain, seizure thresholds; Toxicity, convulsions.)
Thirty measurements of intraocular pressure (IOP) were performed on 10 children either with congenital or secondary glaucoma, before and after halothane anesthesia. In 7 normal eyes, IOP decreased a mean of 3 mm Hg, while in 23 glaucomatous eyes, mean IOP decreased from 43 to 34 mm Hg. In 5 of the 23 glaucomatous eyes, IOP decreased below 25 mm Hg and in only one patient below 21 mm Hg. Our findings indicate that an abnormally elevated IOP during halothane anesthesia suggests a glaucomatous process. A normal IOP during halothane does not absolutely preclude the absence of glaucoma. Intraocular pressure greater than 21 mm Hg during halothane anesthesia should be viewed with suspicion when coupled with other clinical observations of pathologic significance. Awake, sedated IOP measurements appeared to provide a reliable index of glaucoma in the population studied.
Explore the source record for details and available documents.
Diazepam 0.05-0.25 mg/kg increased the dose of lignocaine required to cause seizures in Rhesus monkeys by 24-34%. Spontaneous ventilation was maintained adequately during lignocaine administration following diazepam treatment and no adverse cardiovascular effects occurred. Before the onset of lignocaine-induced seizures in non-treated animals, the animals appeared to be drowsy. However, prior to administration of diazepam masked this effect. Convulsions were controlled by smaller doses of diazepam in non-treated animals than in diazepam-treated animals. Also, the animals that were pretreated with diazepam had a greater duration of depression after seizure.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Because of reports of fluroxene toxicity in man, the effect of phenobarbital treatment on the toxicity and metabolism of fluroxene was studied in 9 rhesus monkeys. Six monkeys that were exposed to a mean calculated alveolar fluroxene concentration of 5.8% for 4-hr periods up to a total of 16 hr showed no evidence of toxicity. Two animals were sacrificed after a single 4-hr exposure to obtain control measures of fluroxene metabolites in tissues. Four monkeys that had previously survived received exposures to fluroxene and 3 monkeys that had no exposure to fluroxene died during fluroxene anesthesia after treatment with phenobarbital (mean time, 3 hr). Toxicity was manifested by arterial hypotension, pulmonary edema, and arterial hypoxemia. Phenobarbital treatment enhanced production of fluroxene metabolites, including the highly toxic trifluoroethanol. Concentrations of trifluoroethanol in mixed-expired gas, blood, and urine, and of total nonvolatile fluorine in blood, urine, and tissues of animals treated with phenobarbital were 2 to 10 times as in control animals. The results suggest that the rhesus monkey is a valuable model for the study of fluroxene pharmacology and that inclusion of an enzyme-inducing challenge in the evaluation of potential toxicity of other anesthetics seems warranted.
The arrhythmogenic dosage of epinephrine, administered by constant intravenous infusion, was measured in five dogs during enflurane, methoxyflurane and halothane anaesthesia. While premature ventricular contractions were observed in only one of five dogs with enflurane and methoxyflurane, epinephrine-induced arrhythmias were seen in all animals during halothane anaesthesia. Epinephrine dosage and the resultant increase in mean arterial blood pressure at which arrhythmias occurred during halothane anaesthesia were significantly less (p less than 0.05) than with the other anaesthetics. These observations indicate that enflurane and methoxyflurane, as compared to halothane, possess relatively less arrhythmogenic potential as sensitizing agents in the presence of increased circulating catecholamines.
Solubility coefficients for seven inhalation anesthetic agnets were determined in maternal and fetal blood at 37 C. Halothane, isoflurane, diethyl ether, and nitrous oxide were significantly more soluble in maternal than in fetal blood, while methoxyflurane, fluroxene, and cyclopropane were significantly less soluble. Reasons for these differences cannot be accounted for by differences in the type or amount of hemoglobin present.
Explore the source record for details and available documents.
Over the past 20 years, more than 300 patients have been anesthetized in the lateral sitting position during neurosurgical procedures in the posterior fossa and the cervical and upper thoracic spine. Since the patient can be placed quickly and easily in the horizontal position, the lateral sitting position has a number of advantages over the conventional sitting position, particularly in the treatment of arterial hypotension and venous air embolism. Furthermore, with the patient in the lateral horizontal position, the surgical procedure can be completed satisfactorily.