Publications by authors named "Richard J Atherley"

Background: We investigated the actions of propofol and isoflurane on nociceptive responses of neurons in the spinal cord.

Methods: We determined nociceptive responses of lumbar neurons in the dorsal horn (<1200 microm) and ventral horn (>1200 microm) of decerebrate rats before and during propofol (1 effective dose, ED(50)) or isoflurane (1 minimum alveolar concentration) anesthesia. During recording of ventral horn neurons, we administered picrotoxin by infusion to determine whether isoflurane and propofol differed in their effects at the gamma aminobutyric acid (GABA) Type A receptors.

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Background: Because of the logistical obstacles to measurement under hyperbaric conditions, the effect of nitrous oxide (N2O) alone on spinal neuronal responses has not been tested. We hypothesized that, like other inhaled anesthetics, N2O would depress spinal neuronal responses to noxious stimulation.

Methods: The lumbar spinal cord was exposed in rats anesthetized with isoflurane.

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Background: Previous work demonstrated that isoflurane and halothane act on the spinal cord rather than on the brain to produce immobility in the face of noxious stimulation. These anesthetics share many effects on specific receptors, and thus do not test the broad applicability of the mediation of immobility by the cord. We sought to test such an applicability by determining whether the cord mediated the immobilizing effects of two aromatic anesthetics that differ greatly in their ability to block N-methyl-d-aspartate receptors.

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The limited potency of nitrous oxide mandates the use of a hyperbaric chamber to produce anesthesia. Use of a hyperbaric chamber complicates anesthetic delivery, ventilation, and electrophysiological recording. We constructed a hyperbaric acrylic-aluminum chamber allowing recording of single unit activity in spinal cord of rats anesthetized only with N(2)O.

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Background: Although volatile anesthetics such as isoflurane can depress sensory and motor neurons in the spinal cord, movement occurring during anesthesia can be coordinated, involving multiple limbs as well as the head and trunk. However, it is unclear whether volatile anesthetics depress locomotor interneurons comprising central pattern generators or disrupt intersegmental central pattern generator coordination.

Methods: Lamprey spinal cords were excised during anesthesia and placed in a bath containing artificial cerebrospinal fluid and D-glutamate to induce fictive swimming.

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We have developed a technique to determine the concentration of volatile anesthetics (halothane, isoflurane and sevoflurane) in blood that is a modification of a method used for volatile anesthetics in Krebs solution. Methylene chloride was the internal standard and chloroform was used to extract the volatile anesthetic from blood. The congealed blood proteins were separated from the chloroform solvent (containing anesthetic) using a two-compartment vial that filtered out the proteinaceous material during centrifuging.

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We have previously observed spontaneous movement when supra-clinical concentrations of isoflurane were selectively delivered to the in situ goat brain. We presently examined whether neurons in the midbrain reticular formation (MRF) remained active during such delivery. Isoflurane (5.

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