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Raines, Douglas E., and Katie B. McClure. "Halothane Interactions with Nicotinic Acetylcholine Receptor Membranes." Anesthesiology 86, no. 2 (February 1, 1997): 476–86. http://dx.doi.org/10.1097/00000542-199702000-00023.
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Background Although it has been suggested that anesthetics alter protein conformational states by binding to nonpolar sites within the interior regions of proteins, the rate and extent to which anesthetics penetrate membrane proteins has not been characterized. The authors report the use of steady-state and stopped-flow spectroscopy to characterize the interactions of halothane with receptor membranes. Methods Steady-state and stopped-flow fluorescence spectroscopy was used to characterize halothane quenching of nicotinic acetylcholine receptor (nAcChoR)-rich membrane intrinsic fluorescence and the rate of isoflurane-induced nAcChoR desensitization. Results At equilibrium, halothane quenched only 54 +/- 1.4% of all tryptophan fluorescence. Diethyl ether failed to reduce fluorescence quenching by halothane, suggesting that it does not bind to the same protein sites as halothane. Stopped-flow fluorescence traces defined two kinetic components of quenching: a fast component that occurred in less than 1 ms followed by a slower biphasic fluorescence decay. Protein unfolding with sodium dodecyl sulfate reduced halothane's Stern-Volmer quenching constant, eliminated the biphasic decay, and rendered fluorescence accessible to quenching by halothane within 1 ms. Functional studies indicate that anesthetic-induced desensitization of nAcChoR occurs in less than 2 ms. Conclusions Unquenchable fluorescence arises from tryptophan residues that are buried within the protein and protected from halothane. Sodium dodecyl sulfate unfolds membrane proteins and allows previously buried fluorescence protein residues to be rapidly and homogeneously quenched by halothane. Halothane quenches protein components of nAcChoR membranes over the same concentration range and time scale that it exerts its functional effects, a finding that is generally consistent with a protein site of action.
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Williams, J. H., M. Holland, J. C. Lee, C. W. Ward, and K. P. Davy. "Effects of BAY K 8644, nifedipine, and low Ca2+ on halothane and caffeine potentiation." Journal of Applied Physiology 71, no. 2 (August 1, 1991): 721–26. http://dx.doi.org/10.1152/jappl.1991.71.2.721.
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The purpose of this investigation was to examine the effects of the Ca2+ agonist BAY K 8644 and the Ca2+ antagonist nifedipine on halothane- and caffeine-induced twitch potentiation of mammalian skeletal muscle. Muscle fiber bundles were taken from normal Landrace pigs and exposed to BAY K 8644 (10 microM), nifedipine (1 microM), and low Ca2+ media administered alone and in combination with halothane (3%) or with increasing concentrations of caffeine (0.5–8.0 mM). Both BAY K 8644 and halothane potentiated twitches by approximately 80%; when they were administered in combination, twitch potentiation was nearly double that caused by either drug alone. In the presence of nifedipine, halothane increased twitches by less than 30%. Low Ca2+ significantly depressed twitches by approximately 25% but also inhibited halothane's inotropic effect. BAY K 8644 augmented caffeine potentiation but only at low caffeine concentrations (0.5–2.0 mM). Nifedipine and low Ca2+ failed to inhibit caffeine's inotropic effects. These results suggest that halothane potentiates twitches via a mechanism that involves or is influenced by extracellular Ca2+.
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Crowder, Michael C., Laynie D. Shebester, and Tim Schedl. "Behavioral Effects of Volatile Anesthetics in Caenorhabditis elegans." Anesthesiology 85, no. 4 (October 1, 1996): 901–12. http://dx.doi.org/10.1097/00000542-199610000-00027.
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Background The nematode Caenorhabditis elegans offers many advantages as a model organism for studying volatile anesthetic actions. It has a simple, well-understood nervous system; it allows the researcher to do forward genetics; and its genome will soon be completely sequenced. C. elegans is immobilized by volatile anesthetics only at high concentrations and with an unusually slow time course. Here other behavioral dysfunctions are considered as anesthetic endpoints in C. elegans. Methods The potency of halothane for disrupting eight different behaviors was determined by logistic regression of concentration and response data. Other volatile anesthetics were also tested for some behaviors. Established protocols were used for behavioral endpoints that, except for pharyngeal pumping, were set as complete disruption of the behavior. Time courses were measured for rapid behaviors. Recovery from exposure to 1 or 4 vol% halothane was determined for mating, chemotaxis, and gross movement. All experiments were performed at 20 to 22 degrees C. Results The median effective concentration values for halothane inhibition of mating (0.30 vol%-0.21 mM), chemotaxis (0.34 vol%-0.24 mM), and coordinated movement (0.32 vol% - 0.23 mM) were similar to the human minimum alveolar concentration (MAC; 0.21 mM). In contrast, halothane produced immobility with a median effective concentration of 3.65 vol% (2.6 mM). Other behaviors had intermediate sensitivities. Halothane's effects reached steady-state in 10 min for all behaviors tested except immobility, which required 2 h. Recovery was complete after exposure to 1 vol% halothane but was significantly reduced after exposure to immobilizing concentrations. Conclusions Volatile anesthetics selectively disrupt C. elegans behavior. The potency, time course, and recovery characteristics of halothane's effects on three behaviors are similar to its anesthetic properties in vertebrates. The affected nervous system molecules may express structural motifs similar to those on vertebrate anesthetic targets.
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Mason, Peggy, Casey A. Owens, and Donna L. Hammond. "Antagonism of the Antinocifensive Action of Halothane by Intrathecal Administration of GABA-A Receptor Antagonists." Anesthesiology 84, no. 5 (May 1, 1996): 1205–14. http://dx.doi.org/10.1097/00000542-199605000-00023.
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Background The hind brain and the spinal cord, regions that contain high concentrations of gamma-aminobutyric acid (GABA) and GABA receptors, have been implicated as sites of action of inhalational anesthetics. Previous studies have established that general anesthetics potentiate the effects of gamma-aminobutyric acid at the GABAA receptor. It was therefore hypothesized that the suppression of nocifensive movements during anesthesia is due to an enhancement of GABAA receptor-mediated transmission within the spinal cord. Methods Rats in which an intrathecal catheter had been implanted 1 week earlier were anesthetized with halothane. Core temperature was maintained at a steady level. After MAC determination, the concentration of halothane was adjusted to that at which the rats last moved in response to tail clamping. Saline, a GABAA, a GABAB, or glycine receptor antagonist was then injected intrathecally. The latency to move in response to application of the tail clamp was redetermined 5 min later, after which the halothane concentration was increased by 0.2%. Response latencies to application of the noxious stimulus were measured at 7-min intervals during the subsequent 35 min. To determine whether these antagonists altered baseline response latencies by themselves, another experiment was conducted in which the concentration of halothane was not increased after intrathecal administration of GABAA receptor antagonists. Results Intrathecal administration of the GABAA receptor antagonists bicuculline (0.3 micrograms) or picrotoxin (0.3, 1.0 micrograms) antagonized the suppression of nocifensive movement produced by the small increase in halothane concentration. In contrast, the antinocifensive effect of the increase in halothane concentration was not attenuated by the GABAB receptor antagonist CGP 35348 or the glycine receptor antagonist strychnine. By themselves, the GABAA receptor antagonists did not alter response latency in rats anesthetized with sub-MAC concentrations of halothane. Conclusions Intrathecal administration of bicuculline or picrotoxin, at doses that do not change the latency to pinch-evoked movement when administered alone, antagonized the suppression of noxious-evoked movement produced by halothane concentrations equal to or greater than MAC. These results suggest that enhancement of GABAA receptor-mediated transmission within the spinal cord contributes to halothane's ability to suppress nocifensive movements.
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VARMA, R. R., R. C. WHITESELL, and M. M. ISKANDARANI. "Halothane Hepatitis Without Halothane." Survey of Anesthesiology 30, no. 4 (August 1986): 205. http://dx.doi.org/10.1097/00132586-198608000-00027.
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Conn, Harold O., and Jonas Skornicki. "Halothane hepatitis sans halothane." Hepatology 5, no. 6 (November 1985): 1238–40. http://dx.doi.org/10.1002/hep.1840050631.
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Hemmings, Hugh C., and Anna I. B. Adamo. "Activation of Endogenous Protein Kinase C by Halothane in Synaptosomes." Anesthesiology 84, no. 3 (March 1, 1996): 652–62. http://dx.doi.org/10.1097/00000542-199603000-00021.
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Background Protein kinase C is a signal transducing enzyme that is an important regulator of multiple physiologic processes and a potential molecular target for general anesthetic actions. However, the results of previous studies of the effects of general anesthetics on protein kinase C activation in vitro have been inconsistent. Methods The effects of halothane on endogenous brain protein kinase C activation were analyzed in isolated rat cerebrocortical nerve terminals (synaptosomes) and in synaptic membranes. Protein kinase C activation was monitored by the phosphorylation of MARCKS, a specific endogenous substrate. Results Halothane stimulated basal Ca2+ dependent phosphorylation of MARCKS (Mr = 83,000) in lysed synaptic membranes (2.1-fold; P< 0.01) and in intact synaptosomes (1.4-fold; P< 0.01). The EC50 for stimulation of MARCKS phosphorylation by halothene in synaptic membranes was 1.8 vol%. A selective peptide protein kinase C inhibitor, but not a protein phosphatase inhibitor (okadaic acid) or a peptide inhibitor of Ca2+/calmodulin-dependent protein kinase II, another Ca2+/-dependent signal transducing enzyme, blocked halothane-stimulated MARCKS phosphorylation in synaptic membranes. Halothane did not affect the phosphorylation of synapsin 1, a synaptic vesicle-associated protein substrate for Ca2+/calmodulin-dependent protein kinase II and AMP-dependent protein kinase, in synaptic membranes or intact synaptosomes subjected to KC1-evoked depolarization. However, halothane stimulated synapsin 1 phosphorylation evoked by ionomycin (a Ca2+ ionophore that permeabilizes membranes to Ca2+) in intact synaptosomes. Conclusions Halothane acutely stimulated basal protein kinase C activity in synaptosomes when assayed with endogenous nerve terminal substrates, lipids, and protein kinase C. This effect appeared to be selective for protein kinases C, because two other structurally similar second messenger-regulated protein kinases were not affected. Direct determinations of anesthetic effects on endogenous protein kinase C activation, translocation, and/or down-regulation are necessary to determine the ultimate effect of anesthetics on the protein kinase C signaling pathway in intact cells.
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Alkire, Michael T., Chris J. D. Pomfrett, Richard J. Haier, Marc V. Gianzero, Candice M. Chan, Bradley P. Jacobsen, and James H. Fallon. "Functional Brain Imaging during Anesthesia in Humans." Anesthesiology 90, no. 3 (March 1, 1999): 701–9. http://dx.doi.org/10.1097/00000542-199903000-00011.
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Background Propofol and isoflurane anesthesia were studied previously with functional brain imaging in humans to begin identifying key brain areas involved with mediating anesthetic-induced unconsciousness. The authors describe an additional positron emission tomography study of halothane's in vivo cerebral metabolic effects. Methods Five male volunteers each underwent two positron emission tomography scans. One scan assessed awake-baseline metabolism, and the other scan assessed metabolism during halothane anesthesia titrated to the point of unresponsiveness (mean +/- SD, expired = 0.7+/-0.2%). Scans were obtained using a GE2048 scanner and the F-18 fluorodeoxyglucose technique. Regions of interest were analyzed for changes in both absolute and relative glucose metabolism. In addition, relative changes in metabolism were evaluated using statistical parametric mapping. Results Awake whole-brain metabolism averaged 6.3+/-1.2 mg x 100 g(-1) x min(-1) (mean +/- SD). Halothane reduced metabolism 40+/-9% to 3.7+/-0.6 mg x 100 g(-1) x min(-1) (P< or =0.005). Regional metabolism did not increase in any brain areas for any volunteer. The statistical parametric mapping analysis revealed significantly less relative metabolism in the basal forebrain, thalamus, limbic system, cerebellum, and occiput during halothane anesthesia. Conclusions Halothane caused a global whole-brain metabolic reduction with significant shifts in regional metabolism. Comparisons with previous studies reveal similar absolute and relative metabolic effects for halothane and isoflurane. Propofol, however, was associated with larger absolute metabolic reductions, suppression of relative cortical metabolism more than either inhalational agent, and significantly less suppression of relative basal ganglia and midbrain metabolism.
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&NA;. "Halothane see Enflurane/halothane/isoflurane." Reactions Weekly &NA;, no. 351 (May 1991): 6. http://dx.doi.org/10.2165/00128415-199103510-00028.
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Spencer, G. E., N. I. Syed, K. Lukowiak, and W. Winlow. "Halothane-induced synaptic depression at both in vivo and in vitro reconstructed synapses between identified Lymnaea neurons." Journal of Neurophysiology 74, no. 6 (December 1, 1995): 2604–13. http://dx.doi.org/10.1152/jn.1995.74.6.2604.
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1. In the present study we tested the ability of the general anesthetic, halothane, to affect synaptic transmission at in vivo and in vitro reconstructed peptidergic synapses between identified neurons of Lymnaea stagnalis. 2. An identified respiratory interneuron, visceral dorsal 4 (VD4), innervates a number of postsynaptic cells in the central ring ganglia of Lymnaea. Because VD4 has previously been shown to exhibit immunoreactivity for FMRFamide-related peptides, it was hypothesized that these peptides may be utilized by VD4 during synaptic transmission. In the intact, isolated CNS of Lymnaea, we have identified novel connections between VD4 and the pedal A (PeA) cells. We demonstrate that VD4 makes inhibitory connections with the PeA neurons, in particular PeA4, and that these synaptic responses are mimicked by exogenous application of FMRFamide. 3. The synaptic transmission between VD4 and the PeA cells in an intact, isolated CNS preparation was completely blocked in 2%, but not 1% halothanc. Interestingly, the postsynaptic responses (PeA) to exogenous FMRFamide were maintained in the presence of both 1 and 2% halothane. 4. To determine the specificity of the observed responses and to determine the precise synaptic site of anesthetic action, we reconstructed the VD4/PeA synapses in vitro. After isolation from their respective ganglia, both cell types extended processes and established neuritic contact. We demonstrated that not only did the presynaptic neuron reestablish the appropriate inhibitory synapses with the PeA neurons, but that the PeA cells also maintained their responsiveness to exogenous FMRFamide. 5. Superfusion of the in vitro synaptically connected VD4 and PeA cells with 2% halothane completely abolished the synaptic transmission between these cells. However, even higher concentrations of 4% halothane failed to block the responsiveness of the PeA neurons to exogenous FMRFamide. Moreover, both 1 and 2% halothane enhanced the duration of the postsynaptic response to exogenously applied FMRFamide. These data suggest that the halothane-induced depression of synaptic transmission most likely occurred at the presynaptic level. 6. This study provides the first direct evidence that peptidergic transmission in the nervous system may also be susceptible to the actions of general anesthetics. In addition, we utilized a novel approach of in vitro reconstructed synapses for studying the effects of general anesthetics on monosynaptic transmission in the absence of other synaptic influences.
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SATHER, A. P., A. L. SCHAEFER, A. K. W. TONG, C. GARIÉPY, and S. M. ZAWADSKI. "MUSCLE AND RECTAL TEMPERATURE RESPONSE CURVES TO A SHORT-TERM HALOTHANE CHALLENGE IN EIGHT-WEEK-OLD PIGLETS WITH KNOWN GENOTYPE AT THE HALOTHANE LOCUS." Canadian Journal of Animal Science 70, no. 1 (March 1, 1990): 9–14. http://dx.doi.org/10.4141/cjas90-002.
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Each of the three genotypes (NN: normal, halothane negative; Nn: carrier, halothane negative; nn: halothane sensitive) at the halothane locus had a significantly different muscle temperature response curve to a 3-min halothane challenge, while only halothane positive (H+) and negative H−) phenotypes could be distinguished on the basis of the rectal temperature response curves. However, the among animal variation precludes its use as a diagnostic tool for the identification of heterozygous and homozygous normal among halothane negative pigs. Key words: Temperature, halothane gene, swine, genotype
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Staunton, Michael, Cathy Drexler, Phillip G. Schmid, Heather S. Havlik, Antal G. Hudetz, and Neil E. Farber. "Neuronal Nitric Oxide Synthase Mediates Halothane-induced Cerebral Microvascular Dilation." Anesthesiology 92, no. 1 (January 1, 2000): 125. http://dx.doi.org/10.1097/00000542-200001000-00023.
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Background The causes of volatile anesthetic-induced cerebral vasodilation include direct effects on smooth muscle and indirect effects via changes in metabolic rate and release of mediators from vascular endothelium and brain parenchyma. The role of nitric oxide and the relative importance of neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively) are unclear. Methods Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arteriolar diameters were measured using computerized videomicrometry. Vessels were preconstricted with prostaglandin F2alpha (PGF2alpha; halothane group) or pretreated with 7-nitroindazole sodium (7-NINA, specific nNOS inhibitor, 7-NINA + halothane group) or N-nitro-L-arginine methylester (L-NAME; nonselective NOS inhibitor, L-NAME + halothane group) and subsequently given PGF2alpha to achieve the same total preconstriction as in the halothane group. Increasing concentrations of halothane were administered and vasodilation was calculated as a percentage of preconstriction. Results Halothane caused significant, dose-dependent dilation of hippocampal microvessels (halothane group). Inhibition of nNOS by 7-NINA or nNOS + eNOS by L-NAME similarly attenuated halothane-induced dilation at 0.6, 1.6, and 2.6% halothane. The dilation (mean +/- SEM) at 1.6% halothane was 104 +/- 10%, 65 +/- 6%, and 51 +/- 9% in the halothane, 7-NINA + halothane and L-NAME + halothane groups, respectively. The specificity of 7-NINA was confirmed by showing that acetylcholine-induced dilation was not inhibited by 7-NINA but was converted to constriction by L-NAME. Conclusions At clinically relevant concentrations, halothane potently dilates intracerebral arterioles. This dilation is mediated, in part, by neuronally derived nitric oxide. Endothelial NOS does not play a major role in halothane-induced dilation of hippocampal microvessels.
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Hassall, Eric, David M. Israel, Thirumazhisai Gunasekaran, and David Steward. "Halothane Hepatitis in Children." Journal of Pediatric Gastroenterology and Nutrition 11, no. 4 (November 1990): 553–57. http://dx.doi.org/10.1002/j.1536-4801.1990.tb10165.x.
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Halothane hepatitis is now a well‐recognized distinct entity in adults, but there prevails an often‐taught “axiom” that halothane hepatitis “does not occur” in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane‐specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane‐specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane‐specific antibodies obtained.
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Sudo, Roberto T., Gisele Zapata, and Guilherme Suarez-Kurtz. "Studies of the halothane-cooling contractures of skeletal muscle." Canadian Journal of Physiology and Pharmacology 65, no. 4 (April 1, 1987): 697–703. http://dx.doi.org/10.1139/y87-115.
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The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5–2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects of Ca2+-free solutions, of the local anesthetics procaine, procainamide, and lidocaine, and of the muscle relaxant dantrolene on the halothane-cooling contractures are consistent with the proposal that the halothane-cooling contractures result from synergistic effects of halothane and low temperature on Ca sequestration by the sarcoplasmic reticulum. Preliminary results from skinned rabbit muscle fibers support this proposal. The halothane concentrations required for the halothane-cooling contractures of isolated frog or mouse muscles are comparable with those observed in serum of patients during general anesthesia. Accordingly, fascicles dissected from muscle biopsies of patients under halothane anesthesia for programmed surgery develop large contractures when rapidly cooled. The amplitude of these halothane-cooling contractures declined with the time of perfusion of the muscle fascicles in vitro with halothane-free physiological solutions. It is suggested that the halothane-cooling contractures could be used as a simple experimental model for the investigation of the effects of halothane on Ca homeostasis and contractility in skeletal muscle and for study of drugs of potential use in the management of the contractures associated with the halothane-induced malignant hyperthermia syndrome. It is shown that salicylates, but not indomethacin or mefenamic acid, inhibit the halothane-cooling contractures.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 721 (October 1998): 8. http://dx.doi.org/10.2165/00128415-199807210-00024.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 1145 (March 2007): 11. http://dx.doi.org/10.2165/00128415-200711450-00034.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 445 (April 1993): 8. http://dx.doi.org/10.2165/00128415-199304450-00034.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 446 (April 1993): 10. http://dx.doi.org/10.2165/00128415-199304460-00039.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 367 (September 1991): 8. http://dx.doi.org/10.2165/00128415-199103670-00038.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 401 (May 1992): 8. http://dx.doi.org/10.2165/00128415-199204010-00032.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 405 (June 1992): 10. http://dx.doi.org/10.2165/00128415-199204050-00040.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 1217 (August 2008): 17. http://dx.doi.org/10.2165/00128415-200812170-00054.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 1255 (June 2009): 17. http://dx.doi.org/10.2165/00128415-200912550-00048.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 298 (April 1990): 5. http://dx.doi.org/10.2165/00128415-199002980-00024.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 333 (January 1991): 7. http://dx.doi.org/10.2165/00128415-199103330-00035.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 338 (February 1991): 5. http://dx.doi.org/10.2165/00128415-199103380-00025.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 363 (August 1991): 6. http://dx.doi.org/10.2165/00128415-199103630-00025.
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ATLEE, JOHN L. "Halothane." Anesthesiology 67, no. 5 (November 1, 1987): 617–18. http://dx.doi.org/10.1097/00000542-198711000-00001.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 1071 (October 2005): 9. http://dx.doi.org/10.2165/00128415-200510710-00026.
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&NA;. "Halothane." Reactions Weekly &NA;, no. 483 (January 1994): 7. http://dx.doi.org/10.2165/00128415-199404830-00027.
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ASSCHER, A. W. "HALOTHANE." British Journal of Anaesthesia 60, no. 4 (March 1988): 479. http://dx.doi.org/10.1093/bja/60.4.479.
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SPENCE, A. A. "HALOTHANE." British Journal of Anaesthesia 60, no. 4 (March 1988): 479–80. http://dx.doi.org/10.1093/bja/60.4.479-a.
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ASSCHER, A. W. "HALOTHANE." British Journal of Anaesthesia 61, no. 1 (July 1988): 123–24. http://dx.doi.org/10.1093/bja/61.1.123-a.
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SPENCE, A. A. "HALOTHANE." British Journal of Anaesthesia 61, no. 1 (July 1988): 124. http://dx.doi.org/10.1093/bja/61.1.124.
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Summers, Frank W. "Halothane." International Anesthesiology Clinics 36, no. 4 (1998): 83–96. http://dx.doi.org/10.1097/00004311-199803640-00009.
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Ball, C., and R. N. Westhorpe. "Halothane." Anaesthesia and Intensive Care 35, no. 2 (April 2007): 3. http://dx.doi.org/10.1177/0310057x0703500201.
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&NA;. "Halothane see Fentanyl/halothane/vecuronium bromide." Reactions Weekly &NA;, no. 367 (September 1991): 8. http://dx.doi.org/10.2165/00128415-199103670-00039.
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Schmidt, Ulrich, Robert H. G. Schwinger, and Michael Bohm. "Interaction of Halothane with Inhibitory G-proteins in the Human Myocardium." Anesthesiology 83, no. 2 (August 1, 1995): 353–60. http://dx.doi.org/10.1097/00000542-199508000-00016.
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Background Halothane has been reported to possess a catecholamine-sensitizing effect in laboratory animals and in anesthetized patients and to enhance the positive inotropic effect of isoproterenol in human papillary muscle strips. The current study was designed to investigate further the underlying subcellular mechanisms on human myocardium, in particular the mechanism of action of halothane on G-proteins. Methods To investigate the effect of halothane on adenylyl cyclase activity, isoproterenol-, guanylylimidodiphosphate (Gpp(NH)p)-, and forskolin-activated enzyme activities were studied alone and in the presence of halothane in native and manganese-treated membranes. The mechanisms of halothane interaction with inhibitory G-proteins (G1) were studied in adenosine diphosphate-ribosylation studies with pertussis toxin and immunochemical techniques. Results Halothane (1%) augmented isoproterenol- and Gpp(NH)p-stimulated adenylyl cyclase activity but had no effect on forskolin-stimulated enzyme activity. Manganese ions inhibited the stimulating effect of isoproterenol and Gpp(NH)p on adenylyl cyclase activity, but the effect of forskolin remained unchanged in control and halothane-treated membranes. In the presence of pertussis toxin, the effect of isoproterenol and Gpp(NH)p on adenylyl cyclase activity was enhanced, but further stimulation by halothane was abolished. Halothane did not influence the attachment of Gi alpha to the membrane. No effect of halothane on adenosine diphosphate-ribosylation of Gi alpha by pertussis toxin was observed. Conclusions Halothane stimulates adenylyl cyclase activity by inhibiting the function of the inhibitory G-proteins by interfering with the effects of the alpha subunits or beta gamma subunits with the effector. Decreased membrane attachment of Gi alpha in the presence of halothane does not occur. The interaction of alpha and beta gamma subunits is not affected by halothane. Halothane does not impair the binding of pertussis toxin to the Gi alpha-protein.
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SATHER, A. P., and A. C. MURRAY. "THE DEVELOPMENT OF A HALOTHANE-SENSITIVE LINE OF PIGS." Canadian Journal of Animal Science 69, no. 2 (June 1, 1989): 323–31. http://dx.doi.org/10.4141/cjas89-036.
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A halothane-sensitive line of pigs was developed from a Pietrain-Lacombe synthetic line through selection of breeding stock based on their sensitivity to a 4 min, 4.5% halothane challenge. It appears that halothane sensitivity is inherited by a single, autosomal recessive allele (n), that is essentially fully penetrant (0.98) in halothane-sensitive pigs (nn). The gene was fixed within four cycles of selection. Segregation at the halothane locus among the two sexes provided no evidence to suggest differential mortality between the sexes and fit inheritance patterns typical of an autosomal locus. However, litters that originated from nn × nn mating types had 1.3 fewer pigs weaned per litter than those mating types in which at least one parent carried the halothane gene. There was no evidence for any expression of halothane sensitivity in normal pigs (NN) and only infrequent expression in the heterozygote (Nn). Key words: Halothane gene, inheritance, swine
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Diaz-Sylvester, Paula L., Maura Porta, and Julio A. Copello. "Halothane modulation of skeletal muscle ryanodine receptors: dependence on Ca2+, Mg2+, and ATP." American Journal of Physiology-Cell Physiology 294, no. 4 (April 2008): C1103—C1112. http://dx.doi.org/10.1152/ajpcell.90642.2007.
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Malignant hyperthermia (MH) susceptibility is a genetic disorder of skeletal muscle associated with mutations in the ryanodine receptor isoform 1 (RyR1) of sarcoplasmic reticulum (SR). In MH-susceptible skeletal fibers, RyR1-mediated Ca2+ release is highly sensitive to activation by the volatile anesthetic halothane. Indeed, studies with isolated RyR1 channels (using simple Cs+ solutions) found that halothane selectively affects mutated but not wild-type RyR1 function. However, studies in skeletal fibers indicate that halothane can also activate wild-type RyR1-mediated Ca2+ release. We hypothesized that endogenous RyR1 agonists (ATP, lumenal Ca2+) may increase RyR1 sensitivity to halothane. Consequently, we studied how these agonists affect halothane action on rabbit skeletal RyR1 reconstituted into planar lipid bilayers. We found that cytosolic ATP is required for halothane-induced activation of the skeletal RyR1. Unlike RyR1, cardiac RyR2 (much less sensitive to ATP) responded to halothane even in the absence of this agonist. ATP-dependent halothane activation of RyR1 was enhanced by cytosolic Ca2+ (channel agonist) and counteracted by Mg2+ (channel inhibitor). Dantrolene, a muscle relaxant used to treat MH episodes, did not affect RyR1 or RyR2 basal activity and did not interfere with halothane-induced activation. Studies with skeletal SR microsomes confirmed that halothane-induced RyR1-mediated SR Ca2+ release is enhanced by high ATP-low Mg2+ in the cytosol and by increased SR Ca2+ load. Thus, physiological or pathological processes that induce changes in cellular levels of these modulators could affect RyR1 sensitivity to halothane in skeletal fibers, including the outcome of halothane-induced contracture tests used to diagnose MH susceptibility.
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Awad, Joseph A., Jean-Louis Horn, L. Jackson Roberts II, and John J. Franks. "Demonstration of Halothane-induced Hepatic Lipid Peroxidation in Rats by Quantification of Flourine2-Isoprostanes." Anesthesiology 84, no. 4 (April 1, 1996): 910–16. http://dx.doi.org/10.1097/00000542-199604000-00019.
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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. Methods Rats were exposed to 1% halothane or 14% O(2) for 2 h. Pretreatments included phenobarbital, isoniazid, or vehicle. Rats also were exposed to halothane, enflurane, and desflurane at 21% O(2). Lipid peroxidation was assessed by mass spectrometric quantification of F(2)-isoprostanes. Results Exposure of phenobarbital-pretreated rats to 1% halothane at 21% O(2) for 2 h caused liver and plasma F(2)-isoprostane concentrations to increase fivefold compared to nonhalothane control rats. This halothane-induced increase was enhanced by 14% O(2), but hypoxia alone had no significant effect. Alanine aminotransferase activity at 24 h was significantly increased only in the 1% halothane/14% O(2) group. The effect of cytochrome P450 enzyme induction on halothane-induced F(2)-isoprostane production and liver injury was determined by comparing the effects of isoniazid and phenobarbital pretreatment with no pretreatment under hypoxic conditions. Halothane caused 4- and 11-fold increases in plasma and liver F(2)-isoprostanes, respectively, in non-pretreated rats, whereas isoniazid pretreatment had no effect. Phenobarbital pretreatment potentiated halothane-induced lipid peroxidation with 9- and 20-fold increases in plasma and liver F(2)-isoprostanes, respectively. Alanine aminotransferase activity was increased only in this group. At ambient oxygen concentrations, halothane but not enflurane or desflurane, caused F(2)-isoprostanes to increase. Conclusions Specific halothane-induced lipid peroxidation was demonstrated in Sprague-Dawley rats using quantification of F(2)-isoprostanes and was increased by hypoxia and phenobarbital pretreatment, but not isoniazid pretreatment.
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Akata, Takashi, and Walter A. Boyle. "Dual Actions of Halothane on Intracellular Calcium Stores of Vascular Smooth Muscle." Anesthesiology 84, no. 3 (March 1, 1996): 580–95. http://dx.doi.org/10.1097/00000542-199603000-00014.
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Background Halothane has been reported to affect the integrity of intracellular Ca2+ stores in a number of tissues including vascular smooth muscle. However, the actions of halothane on intracellular Ca2+ stores are not yet fully understood. Methods Employing the isometric tension recording method, the action of halothane in isolated endothelium-denuded rat mesenteric arteries under either intact or beta-escinmembrane-permeabilized conditions was investigated. Results Halothane (0.125-5%) produced concentration-dependent contractions in Ca2+ free solution in both intact and membrane-permeabilized muscle strips. Ryanodine treatment or repetitive application of phenylephrine eliminated both caffeine-and halothane-induced contractions in the Ca2+ free solution. When either halothane and caffeine, caffeine and halothane, phenylephrine and halothane, or inositol 1,4,5-triphosphate and halothane were applied consecutively in the Ca2+ free solution in either intact or membrane-permeabilized muscle strips, the contraction induced by application of the second agent of the pair was inhibited compared to application of that agent alone. However, when procaine was applied before and during application of the first agent, the contraction induced by the first agent was inhibited and the contraction induced by the second agent was restored. Heparin inhibited the inositol 1,4,5-triphosphate-mediated contraction, but not contractions induced by halothane or caffeine. Halothane (0.125-5%), applied during Ca2+ loading, produced concentration-dependent inhibition of the caffeine contraction (used to estimate the amount of Ca2+ in the store) in both intact and membrane-permeabilized muscle strips. In contrast, halothane applied with procaine during Ca2+ loading produced concentration-dependent enhancement of the caffeine contraction. This enhancement was observed only in the intact but not in the membrane-permeabilized condition. Conclusions Halothane has two distinct actions on the intracellular Ca2+ stores of vascular smooth muscle, a Ca2+ releasing action and a stimulating action on Ca2+ uptake. Halothane releases Ca2+ from the stores that are sensitive to both caffeine/ryanodine and phenylephrine/inositol 1,4,5-triphosphate through a procaine-sensitive mechanism. The observed inhibitory effect on Ca2+ uptake is probably caused by the Ca2+ uptake after blockade of Ca2+ release may be membrane-mediated.
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Keifer, J. C., H. A. Baghdoyan, and R. Lydic. "Pontine Cholinergic Mechanisms Modulate the Cortical Electroencephalographic Spindles of Halothane Anesthesia." Anesthesiology 84, no. 4 (April 1, 1996): 945–54. http://dx.doi.org/10.1097/00000542-199604000-00023.
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Background Halothane anesthesia causes spindles in the electroencephalogram (EEG), but the cellular and molecular mechanisms generating these spindles remain incompletely understood. The current study tested the hypothesis that halothane-induced EEG spindles are regulated, in part, by pontine cholinergic mechanisms. Methods Adult male cats were implanted with EEG electrodes and trained to sleep in the laboratory. Approximately 1 month after surgery, animals were anesthetized with halothane and a microdialysis probe was stereotaxically placed in the medial pontine reticular formation (mPRF). Simultaneous measurements were made of mPRF acetylcholine release and number of cortical EEG spindles during halothane anesthesia and subsequent wakefulness. In additional experiments, carbachol (88 mM) ws microinjected in the the mPRF before halothane anesthesia to determine whether enhanced cholinergic neurotransmission in the MPRF would block the ability of halothane to induce cortical EEG spindles. Results During wakefulness, mPRF acetylcholine release averaged 0.43 pmol/10 min of dialysis. Halothane at 1 minimum alveolar concentration decreased acetylcholine release (0.25 pmol/10 min) while significantly increasing the number of cortical EEG spindles. Cortical EEG spindles caused by 1 minimum alveolar concentration halothane were not significantly different in waveform, amplitude, or number from the EEG spindles of nonrapid eye movement sleep. Microinjection of carbachol into the mPRF before halothane administration caused a significant reduction in number of halothane-induced EEG spindles. Conclusions Laterodorsal and pedunculopontine tegmental neurons, which provide cholinergic input to the mPRF, play a causal role in generating the EEG spindles of halothane anesthesia.
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Pabelick, Christina M., Yedatore S. Prakash, Mathur S. Kannan, David O. Warner, and Gary C. Sieck. "Effects of Halothane on Sarcoplasmic Reticulum Calcium Release Channels in Porcine Airway Smooth Muscle Cells." Anesthesiology 95, no. 1 (July 1, 2001): 207–15. http://dx.doi.org/10.1097/00000542-200107000-00032.
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Background Volatile anesthetics relax airway smooth muscle (ASM) by altering intracellular Ca2+ concentration ([Ca2+]i). The authors hypothesized that relaxation is produced by decreasing sarcoplasmic reticulum Ca2+ content via increased Ca2+ "leak" through both inositol trisphosphate (IP3) and ryanodine receptor channels. Methods Enzymatically dissociated porcine ASM cells were exposed to acetylcholine in the presence or absence of 2 minimum alveolar concentration (MAC) halothane, and IP3 levels were measured using radioimmunoreceptor assay. Other cells were loaded with the Ca2+ indicator fluo-3 and imaged using real-time confocal microscopy. Results Halothane increased IP3 concentrations in the presence and absence of acetylcholine. Inhibition of phospholipase C blunted the IP3 response to halothane. Exposure to 2 MAC halothane induced a transient [Ca2+]i response, suggesting depletion of sarcoplasmic reticulum Ca2+. Exposure to 20 microM Xestospongin D, a cell-permeant IP3 receptor antagonist, resulted in a 45+/-13% decrease in the [Ca2+]i response to halothane compared with halothane exposure alone. In permeabilized cells, Xestospongin D or 0.5 mg/ml heparin decreased the [Ca2+]i response to halothane by 65+/-13% and 68+/-22%, respectively, compared with halothane alone. In both intact and permeabilized cells, 20 microM ryanodine blunted the [Ca2+]i response to halothane by 32+/-13% and 39+/-21%, respectively, compared with halothane alone. Simultaneous exposure to Xestospongin D and ryanodine completely inhibited the [Ca2+]i response to halothane. Conclusions The authors conclude that halothane reduces sarcoplasmic reticulum Ca2+ content in ASM cells via increased Ca2+ leak through both IP3 receptor and ryanodine receptor channels. Effects on IP3 receptor channels are both direct and indirect via elevation of IP3 levels.
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Minoda, Yuko, and Evan D. Kharasch. "Halothane-dependent Lipid Peroxidation in Human Liver Microsomes Is Catalyzed by Cytochrome P4502A6 (CYP2A6)." Anesthesiology 95, no. 2 (August 1, 2001): 509–14. http://dx.doi.org/10.1097/00000542-200108000-00037.
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Background Halothane is extensively (approximately 50%) metabolized in humans and undergoes both oxidative and reductive cytochrome P450-catalyzed hepatic biotransformation. Halothane is reduced under low oxygen tensions by CYP2A6 and CYP3A4 in human liver microsome to an unstable free radical, and then to the volatile metabolites chlorodifluoroethene (CDE) and chlorotrifluoroethane (CTE). The free radical is also thought to initiate lipid peroxidation. Halothane-dependent lipid peroxidation has been shown in animals in vitro and in vivo but has not been evaluated in humans. This investigation tested the hypothesis that halothane causes lipid peroxidation in human liver microsomes, identified P450 isoforms responsible for halothane-dependent lipid peroxidation, and tested the hypothesis that lipid peroxidation is prevented by inhibiting halothane reduction. Methods Halothane metabolism was determined using human liver microsomes or cDNA-expressed P450. Lipid peroxidation was quantified by malondialdehyde (MDA) formation using high-pressure liquid chromatography-ultraviolet analysis of the thiobarbituric acid-MDA adduct. CTE and CDE were determined by gas chromatography-mass spectrometry. Results Halothane caused MDA formation in human liver microsomes at rates much lower than in rat liver microsomes. Human liver microsomal MDA production exhibited biphasic enzyme kinetics, similar to CDE and CTE production. MDA production was inhibited by the CYP2A6 inhibitor methoxsalen but not by the CYP3A4 inhibitor troleandomycin. Halothane-dependent MDA production was catalyzed by cDNA-expressed CYP2A6 but not CYP3A4 or P450 reductase alone. CYP2A6-catalyzed MDA production was inhibited by methoxsalen or anti-CYP2A6 antibody. Conclusions Halothane causes lipid peroxidation in human liver microsomes, which is catalyzed by CYP2A6, and inhibition of halothane reduction prevents halothane-dependent lipid peroxidation in vitro.
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Rezaiguia-Delclaux, Saida, Christian Jayr, Deng Feng Luo, Nor-Eddine Saidi, Michel Meignan, and Philippe Duvaldestin. "Halothane and Isoflurane Decrease Alveolar Epithelial Fluid Clearance in Rats." Anesthesiology 88, no. 3 (March 1, 1998): 751–60. http://dx.doi.org/10.1097/00000542-199803000-00027.
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Background Active sodium transport is the primary mechanism that drives alveolar fluid clearance. In the current study, the effects of exposure to halothane and isoflurane on alveolar fluid clearance in rats were evaluated. Methods Rats were exposed to either halothane (0.4% for 6 h or 2% for 2 h) or isoflurane (0.6% for 6 h or 2.8% for 2 h). Reversibility of halothane effects was assessed after 2 h of exposure to 2% halothane. Alveolar and lung liquid clearance were measured by intratracheal instillation of a 5% albumin solution with 1.5 microCi of 125I-albumin, during mechanical ventilation with 100% FiO2 and the halogenated agent. The effect of terbutaline (10(-4) M) added to the albumin solution was tested after 2 h of exposure to 2% halothane. The increase in protein concentration in the airspaces over 1 h was used to evaluate alveolar liquid clearance. Lung liquid clearance was calculated gravimetrically. Results Alveolar liquid clearance rates were decreased by 24%, 30% and 40% compared with controls (P < 0.05) after 2 h of exposure to halothane, 6 h of exposure to halothane, and 6 h of exposure to isoflurane, respectively. After 2 h of exposure to isoflurane, alveolar liquid clearance did not change. In the 2-h halothane exposure group, alveolar liquid clearance returned to the control value 2 h after withdrawal of halothane. Terbutaline increased alveolar liquid clearance by 50% and 89% in the control and 2-h halothane exposure groups, respectively. In all experiments, the same results were obtained for alveolar and lung liquid clearance. Conclusions Halothane and isoflurane caused a reversible decrease in alveolar epithelial fluid clearance. Two hours of exposure to halothane did not alter the stimulatory effect of terbutaline on alveolar liquid clearance.
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Matsumoto, Mishiya, Yasuhiko Iida, Takafumi Sakabe, Takanobu Sano, Toshizo Ishikawa, and Kazuhiko Nakakimura. "Mild and Moderate Hypothermia Provide Better Protection than a Burst-suppression Dose of Thiopental against Ischemic Spinal Cord Injury in Rabbits." Anesthesiology 86, no. 5 (May 1, 1997): 1120–27. http://dx.doi.org/10.1097/00000542-199705000-00016.
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Background Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia. Methods Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined. Results All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord. Conclusions These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.
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Grosenbaugh, D. A., and W. W. Muir. "Cardiorespiratory effects of sevoflurane, isoflurane, and halothane anesthesia in horses." American Journal of Veterinary Research 59, no. 1 (January 1, 1998): 101–6. http://dx.doi.org/10.2460/ajvr.1998.59.01.101.
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SUMMARY Objective To determine and compare cardiorespiratory and recovery effects of sevoflurane, isoflurane, and halothane in horses. Animals 8 clinically normal horses (4 mares, 4 geldings), 5 to 12 years old. Procedure Inhalation anesthesia was maintained for 90 minutes with sevoflurane, isoflurane, or halothane. Anesthesia depth was maintained at 1.5 minimum alveolar concentration of halothane, isoflurane, and sevoflurane, then was reduced at 30 and 60 minutes. A surgical plane of anesthesia was reinduced by administration of ketamine or thiopental or by increasing the fractional inspired concentration of sevoflurane. Cardiovascular and pulmonary variables were recorded and compared among inhalation anesthetics. Recovery was monitored, and subjective assessment of recovery quality was performed. Results Hemodynamic and pulmonary indices during sevoflurane anesthesia were similar to those of isoflurane. Cardiac output and systemic arterial pressure decreased less during sevoflurane and isoflurane anesthesia than during halothane anesthesia. After 90 minutes, cardiac output was greater for sevoflurane and isoflurane, respectively, compared with halothane. Mean arterial pressure was similar for all thre anesthetic agents. Respiratory rate for sevoflurane and isoflurane was less than that for halothane. This apparent respiratory depression correlated with greater increase in Paco2 and decreased pH when sevoflurane and isoflurane were compared with halothane. Recovery from sevoflurane anesthesia was qualitatively similar and superior to recovery from isoflurane and halothane, respectively. Time to standing did not differ significantly between sevoflurane and isoflurane, but was shorter than halothane. Conclusions Sevoflurane induced cardiorespiratory effects that were comparable to those of isoflurane and halothane. Cardiac output was greater and respiratory rate was less than that for halothane at 1.5 MAC. Sevoflurane anesthesia was characterized by good control of anesthesia depth during induction, maintenance, and recovery. Recovery time after sevoflurane anesthesia was comparable to that for isoflurane, and recovery was smooth and controlled in a manner consistent with recovery from halothane. (Am J Vet Res 1998;59:101–106)
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Beltran, M., R. Bull, P. Donoso, and C. Hidalgo. "Ca(2+)- and pH-dependent halothane stimulation of Ca2+ release in sarcoplasmic reticulum from frog muscle." American Journal of Physiology-Cell Physiology 271, no. 2 (August 1, 1996): C540—C546. http://dx.doi.org/10.1152/ajpcell.1996.271.2.c540.
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The effect of halothane on calcium release kinetics was studied in triad-enriched sarcoplasmic reticulum vesicles from frog skeletal muscle. Release from vesicles passively equilibrated with 3 mM 45CaCl2 was measured in the millisecond time range by use of a fast-filtration system. Halothane (400 microM) increased release rate constants at pH 7.1 and 7.4 as a function of extravesicular pCa. In contrast, halothane at pH 6.8 produced the same stimulation of release from pCa 7.0 to 3.0; no release took place in these conditions in the absence of halothane. Halothane shifted the calcium activation curve at pH 7.1, but not at pH 7.4, to the left and increased channel open probability at pH 7.1 in the cis pCa range of 7.0 to 5.0. These results indicate that cytosolic pCa and pH modulate the stimulatory effects of halothane on calcium release. Furthermore, halothane stimulated release in frog skeletal muscle at low pH and resting calcium concentration, indicating that in frog muscle halothane can override the closing of the release channels produced by these conditions, as it does in malignant hyperthermia-susceptible porcine muscle.
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Duke, Adrian M., Philip M. Hopkins, Jane P. Halsal, and Derek S. Steele. "Mg2+Dependence of Halothane-induced Ca2+Release from the Sarcoplasmic Reticulum in Skeletal Muscle from Humans Susceptible to Malignant Hyperthermia." Anesthesiology 101, no. 6 (December 1, 2004): 1339–46. http://dx.doi.org/10.1097/00000542-200412000-00014.
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Background Recent work suggests that impaired Mg(2+) regulation of the ryanodine receptor is a common feature of both pig and human malignant hyperthermia. Therefore, the influence of [Mg(2+)] on halothane-induced Ca(2+) release from the sarcoplasmic reticulum was studied in malignant hyperthermia-susceptible (MHS) or -nonsusceptible (MHN) muscle. Methods Vastus medialis fibers were mechanically skinned and perfused with solutions containing physiologic (1 mm) or reduced concentrations of free [Mg(2+)]. Sarcoplasmic reticulum Ca(2+) release was detected using fura-2 or fluo-3. Results In MHN fibers, 1 mm halothane consistently did not induce sarcoplasmic reticulum Ca(2+) release in the presence of 1 mm Mg(2+). It was necessary to increase the halothane concentration to 20 mm or greater before Ca release occurred. However, when [Mg(2+)] was reduced below 1 mm, halothane became an increasingly effective stimulus for Ca(2+) release; e.g., at 0.4 mm Mg(2+), 58% of MHN fibers responded to halothane. In MHS fibers, 1 mm halothane induced Ca(2+) release in 57% of MHS fibers at 1 mm Mg(2+). Reducing [Mg(2+)] increased the proportion of MHS fibers that responded to 1 mm halothane. Further experiments revealed differences in the characteristics of halothane-induced Ca(2+) release in MHS and MHN fibers: In MHN fibers, at 1 mm Mg(2+), halothane induced a diffuse increase in [Ca(2+)], which began at the periphery of the fiber and spread slowly inward. In MHS fibers, halothane induced a localized C(2+)a release, which then propagated along the fiber. However, propagated Ca(2+) release was observed in MHN fibers when halothane was applied at an Mg(2+) concentration of 0.4 mm or less. Conclusions When Mg(2+) inhibition of the ryanodine receptor is reduced, the halothane sensitivity of MHN fibers and the characteristics of the Ca release process approach that of the MHS phenotype. In MHS fibers, reduced Mg(2+) inhibition of the ryanodine receptor would be expected to have a major influence on halothane sensitivity. The Mg dependence of the halothane response in MHN and MHS may have important clinical implications in circumstances where intracellular [Mg(2+)] deviates from normal physiologic concentrations.