A precision machine for mounting tissue for Mohs micrographic surgery.

Background: Mounting specimens onto chucks, so the cryostat knife follows the exact path of the surgeon's knife, poses difficulties even for experienced histotechnologists. Oftentimes, the frozen planar surface of the tissue falls at an angle that requires gimballing the chuck holder to compensate.

Objective: To demonstrate the use of a precision tissue mounting machine and associated fast freezing chucks.

Anesthetic-induced alteration of Ca2+ homeostasis in neural cells: a temperature-sensitive process that is enhanced by blockade of plasma membrane Ca2+-ATPase isoforms.

Background: Many inhalation anesthetics at clinically relevant concentrations inhibit plasma membrane Ca2+-adenosine triphosphatase (PMCA) ion pumping in brain synaptic membranes and in cultured cells of neural origin. In this study, the authors investigated the effect of inhalation anesthetics on cytosolic calcium homeostasis in cortical neurons maintained at physiologic and room temperatures and on cortical neurons and pheochromocytoma cells with antisense blockade of specific PMCA isoforms.

Methods: Using Ca2+-specific confocal microfluorimetry, the anesthetic effects on Ca2+ dynamics were examined in mouse embryonic cortical neurons in association with ligand-stimulated Ca2+ influx.

Development of a new standard laboratory protocol for estimating the field attenuation of hearing protection devices. Part III. The validity of using subject-fit data.

The mandate of ASA Working Group S12/WG11 has been to develop "laboratory and/or field procedure(s) that yield useful estimates of field performance" of hearing protection devices (HPDs). A real-ear attenuation at threshold procedure was selected, devised, tested via an interlaboratory study, and incorporated into a draft standard that was approved in 1997 [J. D.

Halothane alters electrical activity and calcium dynamics in cultured mouse cortical, spinal cord, and dorsal root ganglion neurons.

Halothane inhibits neural plasma membrane Ca(2+)-ATPase, a pump that ejects Ca2+ from the cell after influx through voltage- or ligand-activated channels. Intracellular microelectrode recordings in mouse embryonic cortical and spinal cord neurons showed that halothane and eosin, a pump inhibitor, prolonged repolarization associated with spontaneous bursts of depolarization. These agents also prolonged the repolarization phases of electrically induced action potentials and of capsaicin-mediated Ca(2+)-dependent depolarization in mouse adult dorsal root ganglion neurons.

Alcohol pretreatment does not affect bupivacaine pharmacokinetics in the pig.

We investigated whether alcohol pretreatment sufficient to cause fatty liver change would affect the disposition of bupivacaine after i.v. administration in pigs.

Demonstration of halothane-induced hepatic lipid peroxidation in rats by quantification of F2-isoprostanes.

Background: Halothane can be reductively metabolized to free radical intermediates that may initiate lipid peroxidation. Hypoxia and phenobarbital pretreatment in Sprague-Dawley rats increases reductive metabolism of halothane. F(2)-isoprostanes, a novel measure of lipid peroxidation in vivo, were used to quantify halothane-induced lipid peroxidation in rats.

Increased anesthetic requirements for isoflurane, halothane, enflurane and desflurane in obese Zucker rats are associated with insulin-induced stimulation of plasma membrane Ca(2+)-ATPase.

A wide spectrum of structurally disparate inhalational anesthetics reduce brain synaptic plasma membrane Ca(2+)-ATPase (PMCA) activity, whereas phospholipid methyltransferase I (PLMTI) is enhanced by anesthetics. Several rat models with incidental or disease-induced reduction of PMCA and enhancement of PLMTI activities manifest increased sensitivity to inhalational anesthetics. Because insulin is known to stimulate PMCA, anesthetic requirements in hyperinsulinemic obese Zucker rats (fa/fa) and in normoinsulinemic lean Zucker heterozygotes (fa/+) were examined, and brain synaptic PMCA and PLMTI activities were determined in both genotypes.

Reduced anesthetic requirements in aged rats: association with altered brain synaptic plasma membrane Ca(2+)-ATPase pump and phospholipid methyltransferase I activities.

Aging is associated with a decrease in anesthetic requirements. Animal models of aging manifest alteration of brain Ca2+ homeostasis and increased methyltransferase I (PLMTI) activity. In this study we evaluated concurrently anesthetic requirements and brain plasma membrane Ca(2+)-ATPase (PMCA) and PLMTI activities in young and aged rats.

Experimental pain stimulates respiration and attenuates morphine-induced respiratory depression: a controlled study in human volunteers.

Although evidence is lacking, clinical experience suggests that pain stimulation acts as a respiratory stimulant and antagonises opioid-induced respiratory depression. The present study examined the effects of experimental pain stimulation on the ventilatory response to CO2 and morphine-induced respiratory depression. Pain was induced by a modification of the Tourniquet Pain Technique and changes in ventilatory parameters were registered through monitoring of the CO2 response of tidal volume, minute ventilation, respiratory rate and mouth occlusion pressure.

[Ketamine in the management of intractable phantom pain].

A case of phantom limb pain, which had not successfully responded to a long list of medical therapy or neurosurgery, is presented. After oral ketamine treatment was instituted the patient became free of pain. A possible mode of action is described.

Substance P level is increased in the cholesterol induced anaphylactoid reaction in the pig.

The role of substance P (SP) in cholesterol-induced anaphylactoid reaction was investigated in 13 Landrace pigs. Pigs were anesthetized with sodium thiopental and ventilation was controlled with 70% nitrous oxide in oxygen. A Swan-Ganz catheter and a carotid arterial line were placed to monitor the hemodynamic data.

Inhibition of plasma membrane Ca(2+)-ATPase pump activity in cultured C6 glioma cells by halothane and xenon.

We have compared the effect of two inhalational anesthetics, halothane and xenon, on Ca(2+)-ATPase (PMCA) pumping activity in plasma membrane vesicles prepared from cultured rat C6 glioma cells. Halothane, at concentrations ranging from 0.5 to 1.

Stable inhibition of brain synaptic plasma membrane calcium ATPase in rats anesthetized with halothane.

Background: The authors recently showed that plasma membrane Ca(2+)-ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose-related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia.

Methods: Three treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom.

Halothane, isoflurane, xenon, and nitrous oxide inhibit calcium ATPase pump activity in rat brain synaptic plasma membranes.

Background: Perturbation of neuronal calcium homeostasis may alter neurotransmission in the brain, a phenomenon postulated to characterize the anesthetic state. Because of the central role of plasma membrane Ca(2+)-ATPase (PMCA) in maintaining Ca2+ homeostasis, the authors examined the effect of several inhalational anesthetics on PMCA function in synaptic plasma membranes (SPM) prepared from rat brain.

Methods: Ca(2+)-ATPase pumping activity was assessed by measurement of ATP-dependent uptake of Ca2+ by SPM vesicles.

Nitrous oxide and xenon enhance phospholipid-N-methylation in rat brain synaptic plasma membranes.

Halothane and isoflurane increase the rate of phospholipid methylation (PLM) in rat brain synaptosomal membranes, a process linked to the coupling of neuronal excitation to neurotransmitter release. In contrast, synaptic plasma membrane (SPM) Ca2+ ATPase (PMCA) pumping is reduced by exposure to halothane, isoflurane, xenon and nitrous oxide (N2O). To examine further the relationship between PLM, PMCA and anesthetic action, we investigated the effect of clinically relevant concentrations of two less potent anesthetic gases, N2O and xenon, on PLM in SPM.

Reduced anesthetic requirements, diminished brain plasma membrane Ca(2+)-ATPase pumping, and enhanced brain synaptic plasma membrane phospholipid methylation in diabetic rats: effects of insulin.

We have recently reported that streptozocin (STZ)-induced diabetes in rats was associated with i) reduced Ca2+ pumping by rat brain synaptic plasma membrane Ca(2+)-ATPase (PMCA) and ii) a substantial reduction in the partial pressures of halothane and xenon required to prevent movement in response to stimulation (minimum effective dose or MED). MED for both agents correlated well with the degree of hemoglobin glycation and with PMCA activity. We now report that MEDs for isoflurane, enflurane, and desflurane were also substantially reduced in STZ-diabetic rats, compared with placebo-injected controls.

Diminished brain synaptic plasma membrane Ca(2+)-ATPase activity in spontaneously hypertensive rats: association with reduced anesthetic requirements.

We have recently reported that plasma membrane Ca(2+)-ATPase (PMCA) pumping activity in rat brain synaptic plasma membranes (SPM) was reduced by in vitro or prior in vivo exposure to inhalation anesthetics (IA). In addition, rats with streptozocin-induced diabetes were found to have diminished brain synaptic PMCA pumping and a decrease in the partial pressures of several IA required to prevent movement in response to stimulation, defined as the minimum effective dose or MED. Diminished PMCA activity in erythrocytes of spontaneously hypertensive rats (SHR) has been noted.

The effect of hepatectomy and plasma cholinesterase inhibition on cocaine metabolism and cardiovascular responses in pigs.

To determine the effects of total hepatectomy and inhibition of plasma cholinesterase activity on cocaine metabolism, we measured plasma concentrations of cocaine and its three major metabolites, benzoylecgonine, ecgonine methyl ester, and norcocaine, by high-performance liquid chromatography in three groups of male pigs. Pigs were anesthetized with sodium thiopental and lungs were ventilated with nitrous oxide in oxygen. A right carotid arterial cannula and an internal jugular venous catheter were then inserted for the administration of cocaine and for blood sampling.

Further studies on platelet serotonin transporter binding in depression.

Objective: There is an impressive literature implicating abnormalities in serotonergic neural systems in depression. Many investigators, but not all, have reported low numbers of platelet and brain serotonin (5-HT) transporter sites in drug-free depressed patients. In the present study the authors sought to determine whether the low platelet 5-HT transporter binding in depressed patients is due to previous antidepressant drug exposure.

Alcohol pretreatment alters the metabolic pattern and accelerates cocaine metabolism in pigs.

We investigated whether alcohol pretreatment would affect the disposition and metabolic pattern of intravenously (i.v.) administered cocaine in pigs.

S-adenosyl-L-methionine-mediated enzymatic methylations in the rat retinal membranes.

Enzymatic step-wise methylation of membrane phosphatidylethanolamine (PE) to phosphatidyl-N-methylethanolamine (PME) and then phosphatidyl-choline (PC) has been known to alter membrane properties and responsiveness of cells for activation of receptors by chemical transmitters. Conversion of PE to PME and PME to PC in the presence of S-adenosyl-L-methionine (SAM) are catalyzed by two phospholipid N-methyltransferases, PMT I and PMT II, of which PMT I is the rate limiting enzyme. Retina is a good neuronal model for chemical transmission.

Nature of cholinesterase in the rat retina.

The occurrence of cholinesterases has been demonstrated in retinas of several mammalian species. Histochemical staining techniques indicate that the acetylcholinesterases (AChE) are present in amacrine cells and their neighboring bipolar cells. However, the nature of retinal cholinesterases and their interactions with specific cholinesterase inhibitors are not known.