Relevant bibliographies by topics / Isoflurane

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Academic literature on the topic 'Isoflurane'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Isoflurane"

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Vincent, Robert D., Craig H. Syrop, Bradley J. Van Voorhis, David H. Chestnut, Amy E. T. Sparks, Joan M. McGrath, Won W. Choi, James N. Bates, and Donald H. Penning. "An Evaluation of the Effect of Anesthetic Technique on Reproductive Success after Laparoscopic Pronuclear Stage Transfer." Anesthesiology 82, no. 2 (February 1, 1995): 352–58. http://dx.doi.org/10.1097/00000542-199502000-00005.

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Background Laparoscopic pronuclear stage transfer (PROST) is the preferred method of embryo transfer after in vitro fertilization in many infertility programs. There are scant data to recommend the use or avoidance of any particular anesthetic agent for use in women undergoing this procedure. The authors hypothesized that propofol would be an ideal anesthetic for laparoscopic PROST because of its characteristic favorable recovery profile that includes minimal sedation and a low incidence of postoperative nausea and vomiting. The purpose of the study was to compare propofol and isoflurance with respect to postanesthetic recovery and pregnancy outcomes after laparoscopic PROST. Methods One hundred twelve women scheduled for laparoscopic PROST were randomized to receive either propofol/nitrous oxide or isoflurane/nitrous oxide for maintenance of anesthesia. Results Visual analog scale scores for sedation were lower in the propofol group than in the isoflurance group at all measurements between 30 min and 3 h after surgery. More women experienced emesis and were given an antiemetic during recovery in the isoflurance group than in the propofol group. However, the percentage of pregnancies with evidence of fetal cardiac activity was 54% in the isoflurane group compared with only 30% in the propofol group (P = 0.023). Also, the ongoing pregnancy rate was greater in the isoflurane group than in the propofol group (54% vs. 29%, P = 0.014). Conclusions Propofol/nitrous oxide anesthesia was associated with lower clinical and ongoing pregnancy rates compared with isoflurane/nitrous oxide anesthesia.
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Dupin, Jo�o Bosco, Alfredo In�cio Fiorelli, Jo�o Henrique Dupin, Ana Elisa Dupin, Isabela Maria Dupin, and Otoni M. Gomes. "Effects of Clonidine and Isoflurane on the Myocardial Contractility Behavior of Isolated Rat Hearts." Heart Surgery Forum 13, no. 1 (February 11, 2010): 57. http://dx.doi.org/10.1532/hsf98.20091136.

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Isoflurane is chosen as an anesthesia drug for cardiac surgeries, and its effectiveness and safety have been proved in countless clinical studies. Clonidine, a central -agonist, has recently been added to isoflurane to attenuate sympathetic hyperactivity by acting directly on its site of origin in the central nervous system. The ability of 2-adrenoceptor agonists to inhibit central sympathetic outflow may benefit patients at risk of myocardial damage by improving myocardial oxygen demand and the supply ratio and contributing to hemodynamic stability. We investigated the effects of clonidine and isoflurane, alone and in combination, on the myocardial contractility of isolated rat hearts and found that use of clonidine plus isoflurane decreased the systolic pressure somewhat, but use of the drugs separately did not exhibit this effect. Clonidine plus isoflurane did not affect +(dP/dt)max, but it did decrease -(dP/dt)max significantly compared with the use of isoflurane alone. These results indicate that clonidine and isoflurane have the capacity to interact with each other. The capacity of clonidine to decrease isoflurane's inotropic effect could theoretically contribute to improving the myocardial oxygen demand and the supply ratio, decreasing surgical stress, and benefiting patients at risk of myocardial damage.
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Raines, Douglas E., and Vinu T. Zachariah. "Isoflurane Increases the Apparent Agonist Affinity of the Nicotinic Acetylcholine Receptor." Anesthesiology 90, no. 1 (January 1, 1999): 135–46. http://dx.doi.org/10.1097/00000542-199901000-00019.

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Background Volatile general anesthetics increase agonist-mediated ion flux through the gamma-aminobutyric acid(A), glycine, and 5-hydroxytryptamine3 (5-HT3) receptors. This action reflects an anesthetic-induced increase in the apparent agonist affinity of these receptors. In contrast, volatile anesthetics block ion flux through the nicotinic acetylcholine receptor (nAcChoR). The authors tested the hypothesis that in addition to blocking ion flux through the nAcChoR, isoflurane also increases the apparent affinity of the nAcChoR for agonist. Methods Nicotinic acetylcholine receptors were obtained from the electroplax organ of Torpedo nobiliana. The apparent agonist affinity of the nAcChoR was determined using a new stopped-flow fluorescence assay. This assay derives the apparent agonist affinity of the nAcChoR from the apparent rates with which agonists convert nAcChoRs from the resting state to the desensitized state. Results Isoflurane significantly increased the apparent affinity (decreased the apparent dissociation constant) of acetylcholine for the nAcChoR at clinically relevant concentrations. The apparent dissociation constant decreased exponentially with the isoflurane concentration from a control value of 44+/-4 microM to 1.0+/-0.1 microM in the presence of 1.5 mM isoflurane, the highest concentration studied. Conclusions Isoflurane increases the apparent agonist affinity of the nAcChoR; however, this effect is poorly resolved in ion flux studies because isoflurane also causes channel blockade. The lack of saturation of isoflurane's effect on the apparent agonist affinity even at relatively high isoflurane concentrations argues against a single site of anesthetic action. However, it is consistent with isoflurane interactions with several receptor sites that exhibit a range of anesthetic affinities, sites within the membrane lipid, or both.
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Tanaka, Katsuya, Takashi Kawano, Akiyo Nakamura, Hossein Nazari, Shinji Kawahito, Shuzo Oshita, Akira Takahashi, and Yutaka Nakaya. "Isoflurane Activates Sarcolemmal Adenosine Triphosphate-sensitive Potassium Channels in Vascular Smooth Muscle Cells." Anesthesiology 106, no. 5 (May 1, 2007): 984–91. http://dx.doi.org/10.1097/01.anes.0000265158.47556.73.

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Background Recent evidence indicates that vascular adenosine triphosphate-sensitive potassium (K(ATP)) channels in vascular smooth muscle cells are critical in the regulation of vascular tonus under both physiologic and pathophysiologic conditions. Studies of the interaction of volatile anesthetics with vascular K(ATP) channels have been limited. In the current study, the authors investigated the molecular mechanism of isoflurane's action on vascular K(ATP) channels. Methods Electrophysiologic experiments were performed using cell-attached and inside-out patch clamp techniques to monitor native vascular K(ATP) channels, and recombinant K(ATP) channels comprised of inwardly rectifying potassium channel subunits (Kir6.1) and the sulfonylurea receptor (SUR2B). Isometric tension experiments were performed in rat thoracic aortic rings without endothelium. Results Application of isoflurane (0.5 mM) to the bath solution during cell-attached recordings induced a significant increase in K(ATP) channel activity, which was greatly reduced by pretreatment with a selective inhibitor of protein kinase A (PKA), Rp-cAMPS (100 microM). In inside-out patches, isoflurane did not activate K(ATP) channels. Isoflurane significantly activated wild-type recombinant SUR2B/Kir6.1 in cell-attached patches. Isoflurane-induced activation of wild-type channels was diminished in the PKA-insensitive mutant SUR2B-T633A/Kir6.1, SUR2B-S1465A/Kir6.1, and SUR2B/Kir6.1-S385A. In addition, the authors demonstrated that isoflurane-induced PKA activation was associated with isoflurane-induced decreases in isometric tension in the rat aorta. Conclusion These results indicate that isoflurane activates K(ATP) channels via PKA activation. PKA-dependent vasodilation induced by isoflurane also was observed in isometric tension experiments. Analysis of expressed vascular-type K(ATP) channels suggested that PKA-mediated phosphorylation of both Kir6.1 and SUR2B subunits plays a pivotal role in isoflurane-induced vascular K(ATP) channel activation.
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Herring, Bruce E., Zheng Xie, Jeremy Marks, and Aaron P. Fox. "Isoflurane Inhibits the Neurotransmitter Release Machinery." Journal of Neurophysiology 102, no. 2 (August 2009): 1265–73. http://dx.doi.org/10.1152/jn.00252.2009.

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Despite their importance, the mechanism of action of general anesthetics is still poorly understood. Facilitation of inhibitory GABAA receptors plays an important role in anesthesia, but other targets have also been linked to anesthetic actions. Anesthetics are known to suppress excitatory synaptic transmission, but it has been difficult to determine whether they act on the neurotransmitter release machinery itself. By directly elevating [Ca2+]i at neurotransmitter release sites without altering plasma membrane channels or receptors, we show that the commonly used inhalational general anesthetic, isoflurane, inhibits neurotransmitter release at clinically relevant concentrations, in a dose-dependent fashion in PC12 cells and hippocampal neurons. We hypothesized that a SNARE and/or SNARE-associated protein represents an important target(s) for isoflurane. Overexpression of a syntaxin 1A mutant, previously shown in Caenorhabditis elegans to block the behavioral effects of isoflurane, completely eliminated the reduction in neurotransmitter release produced by isoflurane, without affecting release itself, thereby establishing the possibility that syntaxin 1A is an intermediary in isoflurane's ability to inhibit neurotransmitter release.
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Reinstrup, Peter, Erik Ryding, Lars Algotsson, Kenneth Messeter, Bogi Asgeirsson, and Tore Uski. "Distribution of Cerebral Blood Flow during Anesthesia with Isoflurane or Halothane in Humans." Anesthesiology 82, no. 2 (February 1, 1995): 359–66. http://dx.doi.org/10.1097/00000542-199502000-00006.

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Background Halothane and isoflurane have been shown to induce disparate effects on different brain structures in animals. In humans, various methods for measuring cerebral blood flow (CBF) have produced results compatible with a redistribution of CBF toward deep brain structures during isoflurane anesthesia in humans. This study was undertaken to examine the effects of halothane and isoflurance on the distribution of CBF. Methods Twenty ASA physical status patients (four groups, five in each) anesthetized with either isoflurane or halothane (1 MAC) during normo- or hypocapnia (PaCO2 5.6 or 4.2 kPa (42 or 32 mmHg)) were investigated with a two-dimensional CBF measurement (CBFxenon, intravenous 133xenon washout technique) and a three-dimensional method for measurement of the regional CBF (rCBF) distribution with single photon emission computer-aided tomography (SPECT; 99mTc-HMPAO). In the presentation of SPECT data, the mean CBF of the brain was defined as 100%, and all relative flow values are related to this value. Results The mean CBFxenon level was significantly influenced by the PaCO2 as well as by the anesthetic used. At normocapnia, patients anesthetized with halothane had a mean CBFxenon of 40 +/- 3 (SE) ISI units. With isoflurane, the flow was significantly (P < 0.01, 33 +/- 3 ISI units) less than with halothane. Hypocapnia decreased mean CBFxenon (P < 0.0001) during both anesthetics (halothane 24 +/- 3, isoflurane 13 +/- 2 ISI units). The effects on CBFxenon, between the anesthetics, differed significantly (P < 0.01) also during hypocapnia. There were significant differences in rCBF distribution measured between the two anesthetics (P < 0.05). During isoflurane anesthesia, there was a relative increase in flow values in subcortical regions (thalamus and basal ganglia) to 10-15%, and in pons to 7-10% above average. Halothane, in contrast, induced the highest relative flow levels in the occipital lobes, which increased by approximately 10% above average. The rCBF level was increased approximately 10% in cerebellum with both anesthetics. Changes in PaCO2 did not alter the rCBF distribution significantly. Conclusions There is a difference in the human rCBF distribution between halothane and isoflurane with higher relative flows in subcortical regions during isoflurane anesthesia. However, despite this redistribution, isoflurane anesthesia resulted in a lower mean CBFxenon than did anesthesia with halothane.
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Salman, Iyad A. "Effects of halothane and isoflurane on uterine muscle relaxation during caesarian section." Journal of the Faculty of Medicine Baghdad 54, no. 4 (January 2, 2013): 314–16. http://dx.doi.org/10.32007/jfacmedbagdad.544692.

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Background: The use of nitrous oxide- oxygen alone for the maintenance of general anesthesia in obstetrics is associated with an unacceptable incidence of awareness. We have to add inhalational anesthetic drug. But still there is a complaint from the obstetricians regarding the triggering effect of Hallothane on uterine muscle relaxation Isoflurane is inhalational anesthetic drug and recently brought to Iraq. Objectives : The aim of this study is to evaluate and compare the effect of halothane & isoflurane on uterine muscle contraction in caesarian section. Patient and method: This is a prospective study done on 40 patients in Medical city hospital /Baghdad /Iraq. They were randomly allocated to either the isoflurane group or halothane group ,(each of 20 patients) . Caesarian sections under Standard general anesthesia were donefor all the patints. Time from the delivery of fetus to full uterine contraction was estimated. Also the surgeon graded uterine relaxation on a ten centimeter visual analog scale; the zero point indicated none & the 10 mark sever relaxation respectively.The need for supplementary doses of oxytocin were recorded. Results: The surgeons' assessments of uterine relaxation indicated that it was significantly less with isoflurane (P- value less than 0.05 ) and only one patient in the isoflurane group required additional oxytocin as compared to one patent in halothane group. The time required for complete uterine contraction after delivery in patients given isoflurane revealed significant decrease than patients given halothane (P- value less than 0.05 ). Conclusion: Isoflurane's effect is less than that of halothane on uterine muscle relaxation during caesarian section . This decreases the incidence of awareness during anesthesia.
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Raines, Douglas E., and Vinu T. Zachariah. "Isoflurane Increases the Apparent Agonist Affinity of the Nicotinic Acetylcholine Receptor by Reducing the Microscopic Agonist Dissociation Constant." Anesthesiology 92, no. 3 (March 1, 2000): 775–85. http://dx.doi.org/10.1097/00000542-200003000-00021.

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Background Isoflurane increases the apparent agonist affinity of ligand-gated ion channels. This action reflects a reduction in the receptor's agonist dissociation constant and/or the preopen/open channel state equilibrium. To evaluate the effect of isoflurane on each of these kinetic constants in the nicotinic acetylcholine receptor, the authors analyzed isoflurane's actions on (1) the binding of the fluorescent agonist Dns-C6-Cho to the nicotinic acetylcholine receptor's agonist self-inhibition site and (2) the desensitization kinetics induced by the binding of the weak partial agonist suberyldicholine. Methods The dissociation constant for Dns-C6-Cho binding to the self-inhibitory site was determined using stopped-flow fluorescence spectroscopy. The values of the kinetic constants for agonist binding, channel gating, and desensitization were determined by modeling the suberyldicholine concentration-dependence of the apparent rate of desensitization. Results Isoflurane did not significantly alter the dissociation constant for Dns-C6-Cho binding to the self-inhibitory site even at a concentration as high as 1.5 mM, the highest concentration studied. At this concentration, isoflurane substantially reduced the dissociation constant for suberyldicholine binding to its channel opening site by 97% from 17 +/- 5 microM to 0.5 +/- 0.2 microM, whereas the preopen/open channel state equilibrium was reduced only from 19.1 to 5 +/- 1. Conclusions Isoflurane increases the apparent agonist affinity of the nicotinic acetylcholine receptor primarily by reducing the agonist dissociation constant of the site responsible for channel opening rather than altering channel gating kinetics.
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&NA;. "Isoflurane see Halothane/enflurane/isoflurane." Reactions Weekly &NA;, no. 379 (November 1991): 9. http://dx.doi.org/10.2165/00128415-199103790-00037.

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&NA;. "Isoflurane see Enflurane/halothane/isoflurane." Reactions Weekly &NA;, no. 351 (May 1991): 7. http://dx.doi.org/10.2165/00128415-199103510-00030.

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Dissertations / Theses on the topic "Isoflurane"

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Bradshaw, Jennifer Jean. "Isoflurane : interaction with hepatic microsomal enzymes." Doctoral thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27138.

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lsoflurane interacts with cytochrome P-450 in rat and human hepatic microsomes and the Δ6- and Δ5-desaturases in rat hepatic microsomes. The interaction of isoflurane with cytochrome P-450 results in its metabolism to fluoride ion and organofluorine metabolites. The cytochrome P-450 isozymes catalysing the defluorination of isoflurane were assessed in hepatic microsomes from phenobarbital-, β-naphthoflavone- and pregnenolone-16α-carbonitrilepretreated and untreated rats. One or more of the cytochrome P-450 isozymes induced by phenobarbital and pregnenolone-16α-carbonitrile appear to defluorinate isoflurane, but those induced by β-naphthoflavone do not. From a comparison of the extent of defluorination of isoflurane in hepatic microsomes from phenobarbital- and pregnenolone-16α-carbonitrile-pretreated rats, and their Kₘ and Vₘₐₓ values, it appears that isoflurane is defluorinated by one or more isozymes induced by both phenobarbital and pregnenolone-16α-carbonitrile. The major isozyme is probably cytochrome P-450PCN1. The metabolites of isoflurane were identified in human and phenobarbital-induced rat hepatic microsomes. In microsomes from phenobarbital-pretreated rats, isoflurane is metabolised to fluoride ion and trifluoroacetaldehyde; trifluoroacetic acid is not produced in measureable amounts. The trifluoroacetaldehyde produced binds to microsomal constituents. In human hepatic microsomes, the organofluorine metabolite is identified as trifluoroacetic acid. It is proposed that isoflurane is metabolised by different pathways in human and phenobarbital-induced rat hepatic microsomes. The interaction of isoflurane with the cyanide-sensitive factors was assessed by several criteria. Firstly, using the reoxidation of cytochrome b₅ as an index of fatty acid desaturase activity, isoflurane appears to interact with the Δ6- and/or Δ5-desaturases, but not the Δ9-desaturase. Secondly, these results were confirmed and clarified by the use of direct assays to measure the fatty acid desaturase activity. Using the direct assay, we confirmed that isoflurane did not inhibit the Δ9-desaturase and inhibited Δ6-desaturation of linoleic acid, but not the Δ6-desaturation of α-linolenic acid. The inhibition of the Δ6-desaturation of linoleic acid occurred at low millimolar concentrations of isoflurane. lsoflurane inhibits the Δ5-desaturation of eicosa-8, 11, 14-trienoic acid to a small extent which is only apparent at much higher concentrations of isoflurane than that which inhibits the Δ6-desaturase. Further studies focussed on measurement of the activity of Δ6-desaturase in order to attempt to study the kinetics of the inhibition of the Δ6-desaturase by isoflurane: Δ6-desaturase activity was assessed using hepatic microsomes as the source of the enzyme and linoleic acid as substrate precursor. In the course of these studies, we identified a number of factors that affected the apparent activity of the Δ6-desaturase in hepatic microsomes. These included significant levels of endogenous substrate and competing reactions in the hepatic microsomes. Endogenous substrate levels were quantified and corrected for. We then resorted to computer modelling to extract the kinetics of the Δ6-desaturase free of contributions from acyl-CoA synthetase and lysophospholipid acyltransferase, as well as enzyme decay. The kinetics of isoflurane inhibition of the Δ6-desaturase were then superimposed and studied by computer modelling.
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Jaensch, Susan Mary. "Studies on isoflurane anaesthesia in psittacine birds." Thesis, Jaensch, Susan Mary (2001) Studies on isoflurane anaesthesia in psittacine birds. PhD thesis, Murdoch University, 2001. https://researchrepository.murdoch.edu.au/id/eprint/53177/.

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The aim of the studies reported in this thesis was to describe the effects of isoflurane anaesthesia on the hepatic and respiratory systems in psittacine birds, as these are the two most commonly compromised organ systems during human anaesthesia. The results of these studies will lead to improved understanding of avian anatomy and physiology, and improvement of the current methodologies of anaesthesia administration. Galactose and indocyanine green (ICG) clearances assays were compared with plasma and serum biochemical markers of liver dysfunction in normal chickens and galahs. following coeliotomy and following partial hepatectomy. Coeliotomy did not delay clearance of either compound, but partial hepatectomy resulted in elevation of galactose single point concentrations in chickens and decreased galactose clearance rates in galahs. Serum bile acids were not significantly elevated by either coeliotomy or partial hepatectomy. Alterations in plasma enzymes following coeliotomy and partial hepatectomy were consistent with muscle damage and not hepatic disease. Galactose single point concentrations and galactose clearance tests have the potential to be used both as sensitive, specific assays for screening for hepatic disease and for monitoring the progression of hepatic disease in birds. Isoflurane anaesthesia resulted in no detectable disturbance of hepatic function in either species. The induction of pulmonary oxygen stress and oxygen toxicity was evaluated in budgerigars exposed to either acute, repeated acute or chronic periods of normobaric hyperoxic environments. Assays of a range of enzymic and non-enzymic antioxidants, blood gases and indicators of lipid membrane peroxidation were performed, and the lungs were evaluated by histology and transmission electron microscopy. All durations of oxygen exposure resulted in significant respiratory alkalosis and increased blood and plasma glutathione peroxidase activities. The concentrations of other pulmonary enzymic antioxidants including glutathione reductase and superoxide dismutase were not significantly altered by oxygen exposure. With increasing duration of exposure, the ratio of oxidised to reduced glutathione was significantly increased, while the concentrations of uric acid, a- and y-tocopherols and carotenoids were venous significantly reduced, especially following chronic exposure. Pulmonary concentrations of malonaldehyde and 4-hydroxyalkenal were not significantly increased, while plasma concentrations of 8-epi isoprostane F2ft were significantly elevated following oxygen exposure. Chronic oxygen exposure resulted in significant alteration of the respiratory exchange tissue, with increased parabronchial oedema, epithelial hyperplasia and inflammatory cell infiltration, and significant changes in cell morphology including thickening of endothelial cells, interstitial oedema and ruffling of respiratory epithelial cells. These results indicate that budgerigars develop pulmonary oxygen stress following acute or repeated acute exposure to hyperoxic environments, progressing to pulmonary oxygen toxicity with chronic exposure. Assay of plasma 8-epi isoprostane F2α and blood non-enzymic antioxidants were the most sensitive methods of detecting oxygen stress and oxygen toxicity respectively. The comparative respiratory functional anatomy of sulphur crested cockatoos and galahs studied by evaluation of a respiratory cast of a sulphur crested cockatoo, blood gas analysis, airsac gas-in-gas analysis and spirometry studies in anaesthetised birds. The respiratory functional anatomy of sulphur crested cockatoos was different to that previously described in non-psittacine species, with more extensive cranial and caudal thoracic airsacs and smaller abdominal airsacs. Blood gas analysis indicated significant was arterial and venous hyperoxia as a result of using 100% oxygen as the anaesthetic carrier gas. Ventilation of the clavicular airsac was significantly less than either the cranial or caudal thoracic airsacs. Both endotracheal and caudal thoracic administration of anaesthetic gases provided reliable methods for maintaining anaesthesia and resulted in minimal alteration in respiratory function with the exception of arterial and venous hyperoxia. With both delivery methods, spontaneous respiratory movements and tidal and minute ventilation were not significantly decreased. In contrast, clavicular airsac administration of anaesthesia was not successful either in providing ventilation or maintaining anaesthesia due to lack of spontaneous ventilation of this airsac.
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Mukaida, Kumiko. "Activity of the serotonergic system during isoflurane anesthesia." Kyoto University, 2007. http://hdl.handle.net/2433/135747.

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Miu, Peter. "Isoflurane induced impairment of synaptic transmission in hippocampal neurons of the guinea pig in vitro." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28027.

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The effects of anaesthetic applications of isoflurane on 82 CA₁ neurons were studied in in vitro preparations (guinea pigs) using intracellular recording techniques. Various parameters of their excitability such as membrane electrical properties, action potentials and their afterhyperpolarizing potentials as well as synaptic transmission were determined during bath perfusion of clinically relevant concentrtaions of isoflurane. Concentrations of isoflurane were detected in the bath with ¹⁹fluorine nuclear magnetic resonance techniques, and were found to range between 0.02 and 0.3 mM. No consistent effects on the membrane properties were observed. When synaptic activity was blocked by tetrodotoxin, isoflurane induced a hyperpolarization (3-5 mV) without affecting input conductance which was computed from the voltage responses to injections of hyperpolarizing current pulses and the slopes of current-voltage relations for each cell. Responses to depolarizing pulses revealed that the threshold, amplitude and duration of the evoked spikes were not greatly altered, although repetitive spike firing was suppressed in a dose-dependent manner by isoflurane. Similarly, the amplitude and duration of the long-lasting hyperpolarizations following the elicitation of multiple (4 or 5) spikes were reduced in a reversible and dose-dependent manner. Reductions in amplitude and duration of excitatory and inhibitory postsynaptic potentials evoked by electrical stimulation of stratum radiatum were observed; these effects also were strictly dependent on the dose, as well as on duration of the application. These investigations have revealed that isoflurane interferes with synaptic transmission in the hippocampal slice preparation and suggest that presynaptic actions on transmitter release, in addition to postsynaptic effects
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Adachi, Lauren Naomi Spezia. "Avaliação dos efeitos da acupuntura e da eletroacupuntura em modelo animal de dor neuropática : parâmetros comportamentais e bioquímicos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/169683.

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Dor neuropática (DN) é definida como “dor iniciada ou causada por lesão primária ou disfunção em sistema nervoso”, porém sua prevalência depende do tipo de trauma e da disfunção relacionada. Apesar desta condição dolorosa ser considerada altamente prevalente e debilitante, os tratamentos disponíveis são relacionados a efeitos adversos dificultando a adesão. Devido a isso, buscam-se alternativas não farmacológicas para o tratamento deste tipo de dor, entre elas, as técnicas de neuromodulação periférica, como acupuntura (AC) e eletroacupuntura (EA). Estas técnicas podem ser combinadas com intervenções farmacológicas e não farmacológicas e têm apresentado resultados promissores no tratamento da dor neuropática. No entanto, seus mecanismos de ação não estão totalmente elucidados, desta forma a utilização de modelos animais é de grande valia para o estudo destes mecanismos no tratamento da dor neuropática e da patofisiologia deste tipo de dor crônica. É importante salientar que a aplicação de AC e EA em animais acordados é complexa, visto que gera desconforto e pode alterar a analgesia induzida pelo tratamento. Em muitos estudos a anestesia com isoflurano é utilizada durante a aplicação dos tratamentos, porém sua utilização pode gerar um viés no estudo, considerando a possível interferência do fármaco nos resultados comportamentais e neuroquímicos. Outro importante foco de estudo consiste em comparar as duas técnicas, AC e EA, buscando determinar qual destas é a mais eficaz no tratamento da dor neuropática. Considerando o exposto acima, os objetivos desta tese foram: 1) avaliar os parâmetros comportamentais e neuroquímicos dos efeitos da utilização de anestesia na aplicação de AC e EA em ratos submetidos ao modelo de DN; 2) comparar os efeitos da AC e EA em modelo animal de DN por meio de parâmentros comportamentais, neuroquímicos e histológicos. Considerando os resultados obtidos nesta tese, concluímos que o isoflurano aumenta a analgesia promovida por AC e EA, provavelmente diminuindo o efeito do estresse gerado pela aplicação dos tratamentos em animais acordados, resultado que é corroborado pela diminuição do nível de S100β periférico (marcador de morte neuronal central); Por outro lado, o isoflurano diminuiu os níveis de fator de crescimento neuronal (NGF) no nervo periférico lesado, indicando diminuição do processo de regeneração neural, enquanto a EA aumentou. Ao mesmo tempo, o isoflurano alterou os efeitos dos tratamentos nos comportamentos exploratórios e nos níveis de N-metil D-aspartato em tronco encefáfio e medula espinhal. A AC apresentou-se mais eficaz no tratamento da DN em comparação à EA, porém nenhum dos tratamentos foi capaz de alterar os danos causados pela indução da DN no músculo gastrocnemio esquerdo dos animais demonstrado na histologia. Todavia, este resultado não alterou a analgesia gerada pelos tratamentos.
Neuropathic pain (NP) is defined as "pain initiated or caused by primary injury or dysfunction in the nervous system," but its prevalence depends on the type of trauma and related dysfunction. Although this painful condition is considered to be highly prevalent and debilitating, the available treatments are related to adverse effects, making adherence difficult. Because of this, non-pharmacological alternatives for the treatment of this type of pain are sought, among them, the techniques of peripheral neuromodulation, such as acupuncture (AC) and electroacupuncture (EA). These techniques can be combined with pharmacological and non-pharmacological interventions and have shown promising results in the treatment of neuropathic pain. However, its mechanisms of action are not fully elucidated, so the use of animal models is of great value for the study of these mechanisms in the treatment of neuropathic pain and the pathophysiology of this type of chronic pain. It is important to emphasize that the application of AC and EA in awake animals is complex, since it generates discomfort and can alter the analgesia induced by the treatment. In many studies, anesthesia with isoflurane is used during the application of the treatments, but its use may generate a bias in the study, considering the possible interference of the drug in the behavioral and neurochemical results. Another important focus of the study is to compare the two techniques, AC and EA, seeking to determine which is the most effective in the treatment of neuropathic pain. Considering the above, the objectives of this thesis were: 1) to evaluate the behavioral and neurochemical parameters of the effects of the use of anesthesia in the application of AC and EA in rats submitted to the DN model; 2) to compare the effects of AC and EA on animal model of DN by means of behavioral, neurochemical and morphological parameters. Considering the results obtained in this thesis, we conclude that isoflurane increases the analgesia promoted by AC and EA, probably decreasing the effect of the stress generated by the application of the treatments in agreed animals, a result that is corroborated by the decrease in the level of peripheral S100β (biomarker of central neuronal injury); On the other hand, isoflurane decreased the levels of neural grown factor (NGF) in the injured peripheral nerve, indicating a decrease in the neural regeneration process, while the EA increased. At the same time, isoflurane altered the effects of treatments on exploratory behaviors and N-metil-D-aspartato (NMDA) levels in the brainstem and spinal cord. AC was more effective in the treatment of DN compared to EA, but none of the treatments was able to alter the damage caused by DN induction in the left gastrocnemius muscle of the animals showed in histology. However, this result did not alter the analgesia generated by the treatments.
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6

Sackey, Peter V. "Inhaled sedation with isoflurane in the intensive care unit /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-962-9/.

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Brosnan, Robert Joseph. "Intracranial and cerebral perfusion pressures in isoflurane-anesthetized horses /." Connect to Digital dissertations. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.

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Païta, Lucille. "Caractérisation du canal cationique TRPV1 dans les cardiomyocytes." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1329/document.

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L'infarctus du myocarde, une des causes majeures de mortalité à travers le monde, engendre une mort irréversible du muscle cardiaque suite à une ischémie. Cette ischémie, c'est-à-dire une privation de dioxygène et de nutriments, déclencher un stress réticulaire qui perturbe l'équilibre calcique de la cellule cardiaque. Plusieurs pompes et canaux calciques situés à la membrane plasmique ou réticulaire sont des intervenants clés dans le maintien de l'homéostasie calcique. Parmi eux, il existe des canaux de fuites calciques passives, comme les TRPs, et peu d'informations sont actuellement connus à propos de leur rôle précis au cours de l'infarctus du myocarde.TRPV1 est un canal cationique non sélectif qui est activé par la capsaïcine, le pH et la chaleur nocive (>42°C). Dans le muscle squelettique, nous avions démontré que TRPV1 est situé dans la partie longitudinale du réticulum sarcoplasmique et qu'il répond à différentes stimulations physiologiques et pharmacologiques (Lotteau et al., 2013). Ici, nous nous interrogeons sur un éventuel rôle similaire de TRPV1 dans la physiologie cardiaque. Des analyses biochimiques et des mesures de calcium intracellulaire furent réalisées sur des cardiomyocytes issus de souris WT et KO TRPV1. Nos résultats in vitro montrent que: (a) TRPV1 est exprimé dans les cellules cardiaques; (b) une activation de TRPV1 engendre une réduction de la concentration calcique réticulaire et que (c) TRPV1 pourrait être une cible directe de l'isoflurane.Dans la mesure où TRPV1 peut être modulé par de nombreuses molécules pharmacologiques, il pourrait constituer une cible thérapeutique pour réduire la taille d'infarctus. De nombreuses études antérieures ont déjà mis en évidence un rôle cardioprotecteur de TRPV1 dans le système nerveux entourant le cœur. Le but de cette étude est de décrire le fonctionnement des canaux TRPV1 dans des cardiomyocytes adultes
Acute myocardial infarction (MI), a leading cause of morbidity and mortality worldwide, is the irreversible death of heart muscle secondary to ischemia. This ischemia, i.e. oxygen and nutrients deprivation, triggers a reticular stress disrupting the Ca2+ balance of the cardiac cell. Several Ca2+ pumps and channels located at the sarcolemma or at the reticulum membrane are key players in this maintenance of Ca2+ homeostasis. Among them, we find passive leak channels, such as TRPs and little is known about their precise role in MI.TRPV1 represents a non-selective cation channel that is activated by capsaicin, pH and noxious heat. In skeletal muscle, we previously demonstrated that TRPV1 is located in the longitudinal part of the SR and respond to pharmacological and physiological activations (Lotteau et al., 2013). We questioned here whether TRPV1 might have a similar role in heart physiology. Biochemical analysis and intracellular Ca2+ measurements were performed on cardiomyocytes from wild-type and TRPV1-KO mice. Our in vitro results show that: (i) TRPV1 is expressed in cardiac cells; (ii) an increase in intracellular calcium concentration ([Ca2+]i) is elicited under TRPV1 activation; (iii) TRPV1 could be a direct target of isoflurane. In parallel, our in vivo results indicate that a pharmacological preconditioning by isoflurane decrease the infarct size, probably though activation of TRPV1. According to the fact that TRPV1 activity can be modulated by a lot of pharmacological molecules, TRPV1 may serve as therapeutic target to reduce the infarct size. Most of published data have already evidenced this TRPV1 cardioprotective role in the peripheral heart system. The aim of the present work is to describe how TRPV1 channels behave in adult cardiomyocytes
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Decorps, Anne. "Etude pharmacoéconomique en anesthésie : impact économique d'un réveil rapide après anesthésie au desflurane : étude coût-efficacité." Paris 5, 1999. http://www.theses.fr/1999PA05P156.

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Ferron, Judy-Fay, and Judy-Fay Ferron. "Étude in vivo du "burst-suppression"." Master's thesis, Université Laval, 2009. http://hdl.handle.net/20.500.11794/21020.

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Cette étude résume certains concepts liés à l’anesthésie générale, détaille les mécanismes d’action de l’isoflurane, un anesthésiant volatil, et aborde le phénomène du burst-suppression. Elle vise principalement la compréhension de l’impact de l’isoflurane, à des doses amenant le burst-suppression, sur l’inhibition dans le réseau thalamo-cortical. Nous effectuons des enregistrements intracellulaires de neurones corticaux in vivo et de potentiels de champs locaux à différentes doses d’anesthésiants chez le chat. Conjointement à ces enregistrements, nous appliquons des drogues en iontophorèse en péri-synaptique des neurones enregistrés et nous stimulons les noyaux thalamiques projetant dans les aires corticales enregistrées. Nous suggérons que l’isoflurane amène une diminution de l’inhibition corticale, via une plus grande recapture du glutamate par les glies, ce qui diminue l’activation des interneurones corticaux.
Cette étude résume certains concepts liés à l’anesthésie générale, détaille les mécanismes d’action de l’isoflurane, un anesthésiant volatil, et aborde le phénomène du burst-suppression. Elle vise principalement la compréhension de l’impact de l’isoflurane, à des doses amenant le burst-suppression, sur l’inhibition dans le réseau thalamo-cortical. Nous effectuons des enregistrements intracellulaires de neurones corticaux in vivo et de potentiels de champs locaux à différentes doses d’anesthésiants chez le chat. Conjointement à ces enregistrements, nous appliquons des drogues en iontophorèse en péri-synaptique des neurones enregistrés et nous stimulons les noyaux thalamiques projetant dans les aires corticales enregistrées. Nous suggérons que l’isoflurane amène une diminution de l’inhibition corticale, via une plus grande recapture du glutamate par les glies, ce qui diminue l’activation des interneurones corticaux.
This study summarizes some concepts about general anesthesia, details the mechanisms of action of the volatile anesthetic isoflurane and describes the phenomenon of burst-suppression. It aims at understanding the impact of isoflurane, under doses sufficient to induce burst-suppression, on inhibition in the thalamo-cortical network. We performed intracellular recordings of cortical neurons in vivo and local field potentials under different doses of anesthesia in cats. Additionally, we applied drugs in iontophoresis in the perisynaptic space of the recorded neurons and we stimulated thalamic nuclei projecting to the areas where recordings were performed. We suggest that isoflurane diminishes the cortical inhibition, by an increase of the glutamate uptake by glial cells leading to a diminished activation of cortical interneurons.
This study summarizes some concepts about general anesthesia, details the mechanisms of action of the volatile anesthetic isoflurane and describes the phenomenon of burst-suppression. It aims at understanding the impact of isoflurane, under doses sufficient to induce burst-suppression, on inhibition in the thalamo-cortical network. We performed intracellular recordings of cortical neurons in vivo and local field potentials under different doses of anesthesia in cats. Additionally, we applied drugs in iontophoresis in the perisynaptic space of the recorded neurons and we stimulated thalamic nuclei projecting to the areas where recordings were performed. We suggest that isoflurane diminishes the cortical inhibition, by an increase of the glutamate uptake by glial cells leading to a diminished activation of cortical interneurons.
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Books on the topic "Isoflurane"

1

Lawin, Peter, Hugo Aken, and Christoph Puchstein, eds. Isoflurane. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2.

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Peter, Lawin, Aken H. van 1951-, and Puchstein C. 1951-, eds. Isoflurane. Berlin: Springer-Verlag, 1986.

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Nick, Detlef. Die frühe postoperative Phase nach Isoflurane-Kombinationsnarkosen unter besonderer Berücksichtigung der Sauerstoffsättigung. [s.l.]: [s.n.], 1989.

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Netherlands. Werkgroep van Deskundigen ter Vaststelling van MAC-Waarden. Enflurane, isoflurane, and cyclopropane: Health based recommended occupational exposure limits : report of the Dutch Expert Committee on Occupational Standards, a committee of the Health Council of the Netherlands. Den Haag: Health Council of the Netherlands, 1998.

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Rahm, Sylvia. Die ziliare Aktivität unter dem Einfluss des Narkosegases Isofluran. [s.l.]: [s.n.], 1998.

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Wrede, Birgit. Vergleichsuntersuchungen zur Inhalationsanästhesie mit Isofluran oder Sevofluran beim Kaninchen. Hannover: [s.n.], 1999.

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Hannover, Tierärztliche Hochschule, ed. EEG- Veränderungen während der Allgemeinnarkose mit Isofluran beim Pferd. Hannover: [s.n.], 1995.

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Kreidler, Anton. Beitrag zur Kinetik des Inhalationsnarkotikums Isofluran in der in- und exspiratorischen Atemluft. [s.l.]: [s.n.], 1988.

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Lang, Tatjana. Narkose bei Schildkröten unter besonderer Berücksichtigung von Propofol und Isofluran: Eine klinische Studie. München: Hieronymus, 2002.

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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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Book chapters on the topic "Isoflurane"

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Walle, J. "Newer Anaesthesiological Techniques and Drugs: Progress or Fallacy?" In Isoflurane, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_1.

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Manni, C., G. Pelosi, D. Camaioni, D. Pietrini, F. Rodola, and M. Burza. "Isoflurane in Prolonged and Repeated Anaesthesia." In Isoflurane, 52–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_10.

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Crul, J. F. "Interactions of Volatile Anesthetics and Other Drugs Used in Clinical Practice." In Isoflurane, 56–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_11.

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Merin, R. G. "Isoflurane and Calcium Channel Blockers." In Isoflurane, 67–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_12.

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Jones, R. M. "Isoflurane and Beta-Adrenergic Antagonists." In Isoflurane, 74–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_13.

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Driessen, J. J., J. F. Crul, R. Jansen, and J. Egmond. "Isoflurane and Neuromuscular Blocking Drugs." In Isoflurane, 76–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_14.

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Nöldge, G., N. Krieg, G. Schomburg, B. Baumann, and K. L. Scholler. "Influence of Isoflurane on Muscle Relaxation with Vecuronium in Clinical Anesthesia." In Isoflurane, 83–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_15.

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Aken, H., W. Fitch, T. Brüssel, and C. Puchstein. "Isoflurane in Neurosurgical Patients: Are There Advantages?" In Isoflurane, 87–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_16.

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Fitch, W., D. I. Graham, and H. Aken. "Changes in Regional (Local) Cerebral Blood Flow During Isoflurane-induced Hypotension." In Isoflurane, 95–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_17.

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Messeter, K., L. Algotsson, C. H. Nordström, and E. Ryding. "Cerebrovascular and Metabolic Effects of Isoflurane and Halothane: A Preliminary Report." In Isoflurane, 100–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71230-2_18.

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Conference papers on the topic "Isoflurane"

1

Kabir, Muammar M., Mirza I. Beig, Eugene Nalivaiko, Derek Abbott, and Mathias Baumert. "Isoflurane increases cardiorespiratory coordination in rats." In Smart Materials, Nano-and Micro-Smart Systems, edited by Dan V. Nicolau and Guy Metcalfe. SPIE, 2008. http://dx.doi.org/10.1117/12.810681.

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Gonzalez De Los Santos, F., T. Liu, A. Rinke, A. Ando, G. Pulivendala, and S. Phan. "Isoflurane Anesthetic Attenuates Lung Inflammation and Fibrosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1955.

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Reddy, A. K., K. Namiranian, E. E. Lloyd, R. M. Bryan, G. E. Taffet, and C. J. Hartley. "Effect of isoflurane on aortic impedance in mice." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334387.

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Mehr, Akasha, Syed Irtiza Ali Shah, Muhammad Shaban, Muhammad Shahid, and Malik Muhammad Awais. "Automatic Anesthesia Depth Control System For Isoflurane Concentration." In 2022 19th International Bhurban Conference on Applied Sciences and Technology (IBCAST). IEEE, 2022. http://dx.doi.org/10.1109/ibcast54850.2022.9990208.

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Dunbarr, J. "251. Isoflurane Exposure Case Study: One Company's Approach." In AIHce 2005. AIHA, 2005. http://dx.doi.org/10.3320/1.2758712.

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Kortelainen, J., E. Vayrynen, Xiaofeng Jia, T. Seppanen, and N. Thakor. "EEG-based detection of awakening from isoflurane anesthesia in rats." In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346912.

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Kortelainen, Jukka, Ashwati Vipin, Thow Xin Yuan, Hasan Mir, Nitish Thakor, Hasan Al-Nashash, and Angelo All. "Effect of isoflurane on somatosensory evoked potentials in a rat model." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944572.

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Arai, K., K. Kabayama, J. Ono, H. Nakamura, H. Kimura, and K. Fukase. "Elucidation of isoflurane action mechanism on surgical diabetes using microfluidic device." In THE IRAGO CONFERENCE 2018: A 360-degree Outlook on Critical Scientific and Technological Challenges for a Sustainable Society. Author(s), 2019. http://dx.doi.org/10.1063/1.5089439.

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Macias, Alvaro A., Deborah Culley, Gregory Crosby, Mark A. Perrella, and Rebecca M. Baron. "Inhaled Isoflurane In Mice Ameliorates LPS- AND Ventilator-Induced Lung Injury." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2318.

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Zhang, Dandan, Haiyan Ding, Datian Ye, Xiaofeng Jia, and Nitish Thakor. "Burst Suppression EEG during Hypothermia and Rapid Rewarming in Isoflurane-Anesthetized Rats." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5514818.

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Reports on the topic "Isoflurane"

1

Record, Jeffrey W., C. E. Hargett, and Jr. Isoflurane Anesthesia in the Octodon degus. Fort Belvoir, VA: Defense Technical Information Center, September 1989. http://dx.doi.org/10.21236/ada215492.

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Shen, Yan-Xi, You-Ping Chen, Hong-Cheng Zang, and Gang Shao. Evaluation of the Efficiency of Propofol versus Isoflurane Anesthesia Interventions in Treating Elderly Patients with Postoperative Cognitive Dysfunction: A Protocol for Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0042.

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