Bradycardia during epidural anesthesia in a patient receiving guanfacine.
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Biomedical subjects
Publications and source records attributed to R G Burney.
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The effects of various plasma concentrations of lidocaine on nitrous oxide anesthesia in man and halothane requirements in the dog were studied. The response to incision of the skin was observed in 20 patients who were anesthetized with nitrous oxide, 70% inspired, and oxygen, 30%, plus various plasma levels of lidocaine. In addition, changes in the MAC of halothane in dogs were observed at various levels of lidocaine. In both circumstances lidocaine concentrations of 3 to 6 microgram/ml decreased anesthetic requirements approximately 10 to 28%. At clinically common concentrations of lidocaine, significant decreases in anesthetic requirements should be anticipated.
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Intracranial pressure (ICP) was recorded in 12 patients undergoing craniotomy and 2 patients for carotid arteriogram. ICP did not change in response to the injection of contrast medium but rose significantly and dramatically in response to laryngoscopy and intubation. The increase appeared related to initial ICP and thus may represent exhaustion of compensatory mechanisms in these patients. Special attention must be given to this factor during manipulation of the larynx in neurosurgical patients with raised initial ICP or space-occupying intracranial lesions.
Lidocaine catabolism under N2O anesthesia was evaluated in 5 dogs given a lidocaine infusion of 2 mg/kg/min for 20 minutes. Comparison of results with those of a prior similar study with halothane to be significantly faster in the animals given N2O. The extraction ratio for lidocaine, which did not vary with its arterial concentration, was significantly lower with halothane than with N2O. Decreased hepatic catabolism of drugs such as lidocaine should be anticipated in patients anesthetized with potent inhalation agents such as halothane.
The anesthetic effect of lidocaine was evaluated in rats by determining the change in anesthetic requirement of cyclopropane MAC that was produced by blood concentrations of lidocaine in the clinically useful range. A linear reduction in anesthetic requirement was produced with concentrations up to 1 mug/ml. Further increases in lidocaine up to 5.5 mug/ml resulted in no further decrease in cyclopropane requirement. Lidocaine was found to contribute a maximum MAC fraction of 0.4.
Protein binding of lidocaine (2.5, 5, 10, and 20 microgram/ml in fresh plasma was studied from pH 5.6 to pH 9.8. Percent binding of lidocaine was inversely related to hydrogen-ion and lidocaine concentrations.
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The analgesic properties of lidocaine and morphine were compared in mice using a hot plate stimulus. An analgesic response was defined as an increase in the time required for an animal to attempt to escape by jumping. When compared to saline-treated controls, lidocaine produced a statistically significant dose-related delay in response to heat. Dose-response curves for morphine and lidocaine indicated that morphine has greater potency and efficacy. Naloxone (1.0 mg/kg) reversed the analgesic response due to morphine (10 mg/kg) but had no effect on the analgesia produced by lidocaine (50 mg/kg).