Anesthesia and analgesia
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Anesthesia and analgesia · Oct 1982
Onset and progression of intravenous regional anesthesia with dilute lidocaine.
Intravenous regional anesthesia was induced in seven healthy volunteers using dilute lidocaine solution. Onset and progression were documented by sequential detailed neurologic examinations and compared with changes following intravenous regional administration of normal saline. ⋯ Motor paralysis could precede or follow sensory loss in tissues supplied by the same peripheral nerve; the only consistent finding was persistence of strength in the flexor digitorum profundus of the little finger. The pattern of development of intravenous regional anesthesia was related to the anatomic distribution of the peripheral nerves; it is hypothesized that the primary mechanism of action is block of the small distal nerve branches.
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Anesthesia and analgesia · Oct 1982
Prophylactic intravenous ephedrine infusion during spinal anesthesia for cesarean section.
Ephedrine sulfate was administered to 44 healthy parturients undergoing elective repeat cesarean section under spinal anesthesia. Twenty patients received ephedrine infusion (0.01% solution, beginning with approximately 5 mg/min) immediately after induction of spinal anesthesia to maintain maternal systolic blood pressure between 90% and 100% of the base line systolic blood pressure (mean dose of ephedrine 31.6 mg). Twenty-four patients (control group) received 20 mg of ephedrine as an intravenous bolus, and additional 10-mg increments, if necessary when systolic blood pressure decreased to 80% of the base line systolic blood pressure (mean dose of ephedrine 26.8 mg). ⋯ Nausea and/or vomiting occurred in nine women in the control group and one patient in the infusion group (p less than 0.01). Apgar scores, fetal blood gas tensions, and time for onset of respiration were comparable in the two groups. The results suggest that prophylactic ephedrine infusion is safe and desirable in healthy parturients undergoing cesarean section under spinal anesthesia.
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Anesthesia and analgesia · Oct 1982
Hepatic centrilobular necrosis in rats after exposure to halothane, enflurane, or isoflurane.
Exposure of phenobarbital-pretreated rats to low concentrations of halothane (0.5%) and reduced oxygen tension (FIO2 0.08) resulted in the development of liver necrosis in 51% of the animals. Fasting of rats for 24 hours before the same type of exposure increased the incidence of liver necrosis to 80%. Exposure of fed rats to enflurane (1.5%) and isoflurane (1.4%) in conjunction with low oxygen tensions resulted in no liver necrosis; however, in fasting animals, these same concentrations, when accompanied by low oxygen concentrations, produced an incidence of liver necrosis of 35% and 80%, respectively. ⋯ In this study, in addition to increasing the incidence of toxicity, fasting reduced the glutathione levels and also increased cytochrome P-450 concentrations. Exposure to halothane and to isoflurane, but not to enflurane, further decreased the glutathione level. Perhaps the mechanism of liver toxicity associated with anesthesia, at least in this animal model, is related more directly to severe hypoxia than to a direct toxic intermediate produced as a result of metabolism.