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Relevant bibliographies by topics / Halothane

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Academic literature on the topic 'Halothane'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Halothane"

1

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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Dissertations / Theses on the topic "Halothane"

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Provenat, Véronique. "Les effets toxiques et allergiques de l'halothane." Paris 5, 1989. http://www.theses.fr/1989PA05P046.

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Zhang, Ke. "Cardiac electrophysiology and cardiotoxicity of halothane /." The Ohio State University, 1989. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487676261012213.

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Knight, Trudy Lynn. "The molecular basis of halothane-induced hepatotoxicity." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321782.

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Siadat, Pajouh Majid 1959. "GENERATION OF HALOTHANE INDUCED ANTIBODY IN GUINEA PIGS AND ITS POSSIBLE ROLE IN THE PATHOGENESIS OF HALOTHANE INDUCED LIVER INJURY." Thesis, The University of Arizona, 1986. http://hdl.handle.net/10150/276363.

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LAUNAY, FREDERIC. "Toxicologie de l'halothane." Strasbourg 1, 1991. http://www.theses.fr/1991STR15020.

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Molliex, Serge. "Effets de l'halothane sur les pneumocytes II de rat en culture primaire." Saint-Etienne, 1991. http://www.theses.fr/1991STET6417.

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Vinh, Vu Huu. "Comparative contractile effects of halothane and sevoflurane in rat aorta." Kyoto University, 2001. http://hdl.handle.net/2433/150545.

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Goddard, Helen. "Electrophysiological effects of fentanyl, halothane and isoflurane on guinea-pig isolated ventricular myocytes." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:58f6f4e2-aaa9-4913-a7c2-5568e2f8d72f.

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Torske, Kristine E. "An evaluation of epidural oxymorphone and bupivacaine during halothane anesthesia in dogs." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0026/NQ31906.pdf.

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Darling, John R. "The effects of halothane, isoflurane and sevoflurane on hepatic and renal function." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261937.

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Books on the topic "Halothane"

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Fisher, P. J. Halothane and membrane-bound enzymes. Birmingham: University of Birmingham, 1986.

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Hunt, Philip Andrew. The effect of halothane on phosphatidylcholine hydrolysis in rat cerebral cortex. Birmingham: University of Birmingham, 1987.

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Phillips, Marina. Leistungspsychologische und elektroenzephalographische Vigilanzmessungen der unmittelbaren postoperativen Phase nach standardisierten Inhalationsnarkosen mit Isofluran und Halothan. [s.l.]: [s.n.], 1989.

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Gerdes, Christoph. Die Rolle des Serotoninsystems bei der Induktion der durch Halothan ausgelösten malignen Hyperthermie beim Schwein. Hannover: [s.n.], 1992.

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Schurian, Felicitas. Zum Einsatz von Sevofluran beim Syrischen Goldhamster (Mesocricetus auratus) - eine Vergleichsstudie zu Halothan und Isofluran. München: Hieronymus, 2000.

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6

Prüssmann, Joachim. Einfluss einer Prämedikation mit Diazepam oder Promethazin auf die Biotransformation von Halothan beim Menschen und bei der Ratte. [s.l.]: [s.n.], 1985.

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7

Breisgau, Universität Freiburg im, ed. Der Einfluss von Halothan und Isofluran auf die Blutfliessgeschwindigkeit in der Arteria cerebri media, gemessen mit der Transkraniellen Dopplersonographie. [s.l.]: [s.n.], 1992.

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8

Laichinger, Andreas Hermann. Hepatotoxizität von Halothan: Gaschromatographische Analyse der Atemgase sowie histologische und enzymhistochemische Untersuchungen an der Rattenleber nach Halothanexposition unter normoxischen und hypoxischen Bedingungen. [s.l.]: [s.n.], 1988.

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9

Zur Herzwirkung Von Inhalationsanaesthetica: Der Isolierte Katzenpapillarmuskel Als Myokard-Modell. Springer London, Limited, 2013.

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Mitchel, Marnie. Sevoflurane versus halothane for pediatric ent surgeries: Is the difference clinically significant for patients? 1997.

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Book chapters on the topic "Halothane"

1

Maxwell, Robert A., and Shohreh B. Eckhardt. "Halothane." In Drug Discovery, 297–305. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0469-5_22.

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Gut, Josef. "Molecular Basis of Halothane Hepatitis." In Archives of Toxicology, 3–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-46856-8_1.

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Webb, A. J., O. I. Southwood, and S. P. Simpson. "The Halothane Test in Improving Meat Quality." In Evaluation and Control of Meat Quality in Pigs, 297–315. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3301-9_23.

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Ahern, C. P., W. E. Rempel, J. H. Milde, and G. A. Gronert. "Porcine Malignant Hyperthermia: Dose/Response to Halothane." In Evaluation and Control of Meat Quality in Pigs, 371–78. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3301-9_28.

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Pohl, Lance R., David Thomassen, Neil R. Pumford, Lynn E. Butler, Hiroko Satoh, Victor J. Ferrans, Andrea Perrone, Brian M. Martin, and Jackie L. Martin. "Hapten Carrier Conjugates Associated with Halothane Hepatitis." In Advances in Experimental Medicine and Biology, 111–20. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_12.

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Mosteller, Frederick. "The Safety of Anesthetics: The National Halothane Study." In The Pleasures of Statistics, 69–88. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-77956-0_5.

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Bosnjak, Zeljko J., Sumio Hoka, Lawrence Turner, and John P. Kampine. "Cardiac Protection by Halothane Following Ischemia and Calcium Paradox." In Cell Calcium Metabolism, 593–601. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_61.

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Fischer, K. "The Importance of Reaction Intensity in the Halothane Test." In Evaluation and Control of Meat Quality in Pigs, 379–86. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3301-9_29.

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Kathirvel, Paramasivam, and Alan L. Archibald. "The Halothane Gene, Leanness and Stress Susceptibility in Pigs." In Animal Models — Disorders of Eating Behaviour and Body Composition, 173–90. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9662-6_10.

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Arroyo, J. L., E. Dawson, R. P. Reiner, E. Gonima, and F. Carrascosa. "Effect of Isoflurane and Halothane on the Endocrine System." In Isoflurane, 317–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_49.

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Conference papers on the topic "Halothane"

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Vijayan, Sujith, ShiNung Ching, Patrick L. Purdon, Emery N. Brown, and Nancy J. Kopell. "Biophysical modeling of alpha rhythms during halothane-induced unconsciousness." In 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2013. http://dx.doi.org/10.1109/ner.2013.6696130.

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Sharma, Ashutosh, Sara E. Wilson, and Rob J. Roy. "EEG classification for estimating anesthetic depth during halothane anesthesia." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761515.

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Sharma, Wilson, and Roy. "EEG Classification For Estimating Anesthetic Depth During Halothane Anesthesia." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.592726.

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Letourneau, J. E., and R. Denis. "Variations of horizontal phoria at near during recovery from general anesthesia." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.mr41.

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The purpose of the study was to evaluate recovery from general anesthesia in a day-care surgery unit. A group of forty-three patients underwent surgery under general anesthesia with enflurane (N = 14), isoflurane (N = 10), or halothane (N = 19). Anesthesia lasted 20-95 min (average, 45.3 min). Heterophoria was measured with the Maddox Wing; results are expressed in prism diopters. Patients were measured before anesthesia (condition 1) 1.5, 2.5, and 3.5 h after the end of anesthesia (conditions 2, 3, and 4).

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Pluháčková, Kristýna, Pavel Hobza, Theodore E. Simos, and George Maroulis. "Theoretical Investigation of the Unexpected Red Shift in the Halothane[ellipsis (horizontal)]Acetone Complex." In COMPUTATIONAL METHODS IN SCIENCE AND ENGINEERING: Theory and Computation: Old Problems and New Challenges. Lectures Presented at the International Conference on Computational Methods in Science and Engineering 2007 (ICCMSE 2007): VOLUME 1. AIP, 2007. http://dx.doi.org/10.1063/1.2835999.

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Van Reempts, J., B. Van Deuren, M. Borqers, and F. De Clerck. "R 68 070, A COMBINED TXA2-SYNTHETASE/TXA2-PROSTAGLANDIN ENDOPEROXIDE RECEPTOR INHIBITOR. REDUCES CEREBRAL INFARCT SIZE AFTER PHOTOCHEMICALLY INITIATED THROMBOSIS IN SPONTANEOUSLY HYPERTENSIVE RATS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643470.

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Abstract:

The effects of R 68 070, an oxime-alkane carboxylic acid derivative combining specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule, were investigated in a model of photochemically induced stroke in spontaneously hypertensive rats.Each experimental group was compared with an untreated control group. All animals were anesthetized with halothane in N20/02 and artificially ventilated. After incision of the scalp and stereotaxic positioning of a fibre optic light source, halothane was discontinued. When physiological variables reached normal values, a focal cortical infarction was produced by injection of 10 mg.kg-1 rose bengal and 20 min irradiation of the brain through the intact skull. Four hours later the brains were perfusion fixed and damaged areas measured on consecutive histologic sections. Infarct size was calculated by numerical integration.R 68 070 (40 mg.kg-1 p.o.,-3 h) significantly reduced the cerebral infarct size to 2.32 mm3 compared with 5.78 mm3 in controls (median values; n = 5; p < 0.05). At 2.5 mg.kg-1 the lesion was reduced from 11.75 mm3 in the control group to 7.82 mm3 in the treated group (n = 5; p = 0.095). Serum TXB2 levels were reduced by > 80 %.Production of damage in this model is based upon photodynamic generation of singlet molecular oxygen, resulting in peroxidative endothelial cell injury and subsequent platelet thrombus formation. Protection with R 68 070 can be explained by the anti-thrombotic effect of the compound. The relative contribution to this protective effect of synthetase and receptor blockade by R 68 070 are being investigated.

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7

Borges, Marcos C., Cinzia L. Marchica, Venkatesan Narayanan, and Mara S. Ludwig. "Effect Of Allergen Challenge Under Isoflurane And Halothane Anesthesia In Hyperresponsiveness And Inflammation In A Murine Model Of Allergic Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2882.

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8

ALKIRE, M. T., B. ROOZENDAAL, and L. CAHILL. "TOWARD THE NEUROANATOMIC BASIS OF ANAESTHETIC-INDUCED AMNESIA: HALOTHANE-INDUCED AMNESIA, UNLIKE DIAZEPAM-INDUCED AMNESIA, MAY NOT BE REVERSED WITH BILATERAL LESIONING OF THE BASOLATERAL AMYGDALA." In Proceedings of the Fourth International Symposium. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2000. http://dx.doi.org/10.1142/9781848160231_0040.

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9

Benkovic, Vesna, Nikola Borojević, Nada Oršolić, Gordana Brozović, Anica Horvat Knežević, and Mirta Milić. "Combined exposure to halothane and 1 or 2 Gy ionizing radiation causes synergistic effect in DNA damage in both blood and liver of Swiss albino mice." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/rad.abstr.book.2021.32.16.

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10

Benković, Vesna, Nikola Borojević, Nada Oršolić, Gordana Brozović, Anica Horvat Knežević, and Mirta Milić. "COMBINED EXPOSURE TO HALOTHANE AND 1 OR 2 Gy IONIZING RADIATION CAUSES A SYNERGISTIC EFFECT IN DNA DAMAGE IN THE BLOOD AND LIVER OF SWISS ALBINO MICE." In RAD Conference. RAD Centre, 2021. http://dx.doi.org/10.21175/radproc.2021.10.

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Reports on the topic "Halothane"

1

Kirby, Albert W., Alfred T. Townsend, Carolyn D. Pope, Robert E. Stafford, and Thomas H. Harding. Effects of Halothane Anesthesia on Blood Cholinesterase Activity in Cats. Fort Belvoir, VA: Defense Technical Information Center, July 1989. http://dx.doi.org/10.21236/ada212053.

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2

Knight, Travis, Kenneth J. Stalder, Rodney Goodwin, Steven M. Lonergan, and Donald C. Beitz. Influence of Breed, Gender, and Halothane Genotype on Lipids of longissimus dorsi Muscle of Pigs. Ames (Iowa): Iowa State University, January 2004. http://dx.doi.org/10.31274/ans_air-180814-105.

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