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Journal articles on the topic 'Isoflurane'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 June 2025

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1

Vincent, Robert D., Craig H. Syrop, Bradley J. Van Voorhis, et al. "An Evaluation of the Effect of Anesthetic Technique on Reproductive Success after Laparoscopic Pronuclear Stage Transfer." Anesthesiology 82, no. 2 (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 (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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3

Raines, Douglas E., and Vinu T. Zachariah. "Isoflurane Increases the Apparent Agonist Affinity of the Nicotinic Acetylcholine Receptor." Anesthesiology 90, no. 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, et al. "Isoflurane Activates Sarcolemmal Adenosine Triphosphate-sensitive Potassium Channels in Vascular Smooth Muscle Cells." Anesthesiology 106, no. 5 (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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5

Herring, Bruce E., Zheng Xie, Jeremy Marks, and Aaron P. Fox. "Isoflurane Inhibits the Neurotransmitter Release Machinery." Journal of Neurophysiology 102, no. 2 (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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6

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 (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 &lt; 0.01, 33 +/- 3 ISI units) less than with halothane. Hypocapnia decreased mean CBFxenon (P &lt; 0.0001) during both anesthetics (halothane 24 +/- 3, isoflurane 13 +/- 2 ISI units). The effects on CBFxenon, between the anesthetics, differed significantly (P &lt; 0.01) also during hypocapnia. There were significant differences in rCBF distribution measured between the two anesthetics (P &lt; 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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7

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 (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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8

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 (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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9

&NA;. "Isoflurane see Halothane/enflurane/isoflurane." Reactions Weekly &NA;, no. 379 (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 (1991): 7. http://dx.doi.org/10.2165/00128415-199103510-00030.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1376 (2011): 19. http://dx.doi.org/10.2165/00128415-201113760-00065.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 712 (1998): 10. http://dx.doi.org/10.2165/00128415-199807120-00028.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 723 (1998): 9. http://dx.doi.org/10.2165/00128415-199807230-00028.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1184 (2008): 24–25. http://dx.doi.org/10.2165/00128415-200811840-00075.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 554 (1995): 9. http://dx.doi.org/10.2165/00128415-199505540-00032.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 572 (1995): 9. http://dx.doi.org/10.2165/00128415-199505720-00024.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 586 (1996): 8. http://dx.doi.org/10.2165/00128415-199605860-00029.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 451 (1993): 9. http://dx.doi.org/10.2165/00128415-199304510-00038.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 456 (1993): 9. http://dx.doi.org/10.2165/00128415-199304560-00048.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 472 (1993): 9. http://dx.doi.org/10.2165/00128415-199304720-00043.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 636 (1997): 9. http://dx.doi.org/10.2165/00128415-199706360-00031.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 671 (1997): 10. http://dx.doi.org/10.2165/00128415-199706710-00027.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 793 (2000): 7. http://dx.doi.org/10.2165/00128415-200007930-00023.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 371 (1991): 9. http://dx.doi.org/10.2165/00128415-199103710-00039.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 419 (1992): 8. http://dx.doi.org/10.2165/00128415-199204190-00033.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 893 (2002): 11. http://dx.doi.org/10.2165/00128415-200208930-00039.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 302 (1990): 8. http://dx.doi.org/10.2165/00128415-199003020-00028.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 304 (1990): 8. http://dx.doi.org/10.2165/00128415-199003040-00027.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 310 (1990): 8–9. http://dx.doi.org/10.2165/00128415-199003100-00038.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 945 (2003): 8. http://dx.doi.org/10.2165/00128415-200309450-00022.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1300 (2010): 30. http://dx.doi.org/10.2165/00128415-201013000-00101.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1302 (2010): 31. http://dx.doi.org/10.2165/00128415-201013020-00093.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 505 (1994): 8. http://dx.doi.org/10.2165/00128415-199405050-00038.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 511 (1994): 8. http://dx.doi.org/10.2165/00128415-199405110-00029.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 527 (1994): 8. http://dx.doi.org/10.2165/00128415-199405270-00024.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1336 (2011): 30. http://dx.doi.org/10.2165/00128415-201113360-00097.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1344 (2011): 20. http://dx.doi.org/10.2165/00128415-201113440-00070.

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Warner, David S. "Isoflurane." Journal of Neurosurgical Anesthesiology 2, no. 4 (1990): 319–21. http://dx.doi.org/10.1097/00008506-199012000-00013.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1419 (2012): 30. http://dx.doi.org/10.2165/00128415-201214190-00110.

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&NA;. "Isoflurane." Reactions Weekly &NA;, no. 1429 (2012): 26. http://dx.doi.org/10.2165/00128415-201214290-00093.

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Ball, C., and R. N. Westhorpe. "Isoflurane." Anaesthesia and Intensive Care 35, no. 4 (2007): 467. http://dx.doi.org/10.1177/0310057x0703500401.

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Kissin, Igor, and Simon Gelman. "Isoflurane." Anesthesia & Analgesia 68, no. 6 (1989): 825???826. http://dx.doi.org/10.1213/00000539-198906000-00031.

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Khambatta, Hoshang J., and J. Gilbert Stone. "Isoflurane." Anesthesia & Analgesia 68, no. 6 (1989): 826. http://dx.doi.org/10.1213/00000539-198906000-00032.

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Wei, Huafeng, Ge Liang, and Hui Yang. "Isoflurane preconditioning inhibited isoflurane-induced neurotoxicity." Neuroscience Letters 425, no. 1 (2007): 59–62. http://dx.doi.org/10.1016/j.neulet.2007.08.011.

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Crystal, George J., Edward A. Czinn, Jeffrey M. Silver, and Ramez M. Salem. "Coronary Vasodilation by Isoflurane." Anesthesiology 82, no. 2 (1995): 542–49. http://dx.doi.org/10.1097/00000542-199502000-00024.

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Background Under certain circumstances, isoflurane is associated with coronary artery vasodilation. The objective of the current study was to ascertain whether the rate of administration of isoflurane influences its vasodilating effect in the coronary circulation. Methods Seven open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs; reservoir 1 (control) was supplied with arterial blood free of isoflurane, and reservoir 2 was supplied with blood from an extracorporeal oxygenator, which was provided with 95% O2/5% CO2 gas that passed through calibrated vaporizer. Coronary blood flow (CBF) was measured with Doppler flow transducer. In each dog, isoflurane was administered according to two protocols; abrupt (isoflurane-A) or gradual (isoflurane-G). In isoflurane-A, the left anterior descending coronary artery was switched from reservoir 1 to reservoir 2 after the latter was filled with blood previously equilibrated with 1.4% (1 MAC) isoflurane. In isoflurane-G, the left anterior descending coronary artery was switched to reservoir 2 with vaporizer set at 0% isoflurane; then the vaporizer was adjusted to 1.4% isoflurane, which produced a gradual increase in isoflurane concentration within reservoir 2 that reached a level equivalent to that in isoflurane-A (as evaluated by gas chromatography) by 30 min. CBF during maximally dilating, intracoronary infusion of adenosine served as a reference to assess effects of isoflurane. Results Isoflurane-A caused marked increases in CBF, which, at constant perfusion pressure, reflected pronounced reductions in vascular resistance. These increases in CBF were 80% of those with adenosine. Although isoflurane-G also caused increases in CBF, the increases were only 45% of those caused by isoflurane-A. Conclusions The current findings demonstrate that the extent of coronary vasodilation by isoflurane was not dependent only on its blood concentration but also on the rate at which this blood concentration was achieved; a gradual increase in blood concentration blunted the vasodilator effect. Differences in the rate of administration of isoflurane likely contributed to its widely variable coronary vasodilating effects in previous studies.

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Finegan, Barry A., Manoj Gandhi, Matthew R. Cohen, Donald Legatt, and Alexander S. Clanachan. "Isoflurane Alters Energy Substrate Metabolism to Preserve Mechanical Function in Isolated Rat Hearts following Prolonged No-Flow Hypothermic Storage." Anesthesiology 98, no. 2 (2003): 379–86. http://dx.doi.org/10.1097/00000542-200302000-00018.

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Background Isoflurane enhances mechanical function in hearts subject to normothermic global or regional ischemia. The authors examined the effectiveness of isoflurane in preserving mechanical function in hearts subjected to cardioplegic arrest and prolonged hypothermic no-flow storage. The role of isoflurane in altering myocardial glucose metabolism during storage and reperfusion during these conditions and the contribution of adenosine triphosphate-sensitive potassium (K(atp)) channel activation in mediating the functional and metabolic effects of isoflurane preconditioning was determined. Methods Isolated working rat hearts were subjected to cardioplegic arrest with St. Thomas' II solution, hypothermic no-flow storage for 8 h, and subsequent aerobic reperfusion. The consequences of isoflurane treatment were assessed during the following conditions: (1) isoflurane exposure before and during storage; (2) brief isoflurane exposure during early nonworking poststorage reperfusion; and (3) isoflurane preconditioning before storage. The selective mitochondrial and sarcolemmal K(atp) channel antagonists, 5-hydroxydecanoate and HMR 1098, respectively, were used to assess the role of K(atp) channel activation on glycogen consumption during storage in isoflurane-preconditioned hearts. Results Isoflurane enhanced recovery of mechanical function if present before and during storage. Isoflurane preconditioning was also protective. Isoflurane reduced glycogen consumption during storage under the aforementioned circumstances. Storage of isoflurane-preconditioned hearts in the presence of 5-hydroxydecanoate prevented the reduction in glycogen consumption during storage and abolished the beneficial effect of isoflurane preconditioning on recovery of mechanical function. Conclusions Isoflurane provides additive protection of hearts subject to cardioplegic arrest and prolonged hypothermic no-flow storage and favorably alters energy substrate metabolism by modulating glycolysis during ischemia. The effects of isoflurane preconditioning on glycolysis during hypothermic no-flow storage appears to be associated with activation of mitochondrial K(atp) channels.

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47

Li, Qi Fang, Xiang Rui Wang, Yue Wu Yang та Dian San Su. "Up-regulation of Hypoxia Inducible Factor 1α by Isoflurane in Hep3B Cells". Anesthesiology 105, № 6 (2006): 1211–19. http://dx.doi.org/10.1097/00000542-200612000-00021.

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Background The volatile anesthetic isoflurane induces hypoxia inducible factor (HIF)-1-responsive genes heme oxygenase 1, inducible nitric oxide synthase, and vascular endothelial growth factor (VEGF) expression. Little is known about the extent to which induction of HIF-1alpha is affected by isoflurane. Methods Hep3B cells were exposed to isoflurane at various concentrations (0.5-4%) or for different time periods (2-8 h) at 37 degrees C. HIF-1alpha gene expression and transcriptional activity, heme oxygenase 1, inducible nitric oxide synthase, and VEGF gene expression were quantified. Results Isoflurane induced a time- and concentration-dependent increase in HIF-1alpha protein but not for HIF-1alpha messenger RNA (mRNA) in Hep3B cells. The maximal increase was induced by 2% isoflurane, and the cells incubated with 2% isoflurane for 4-8 h expressed the highest protein. Similarly, HIF-1alpha transcriptional activity was higher in Hep3B cells exposed to 2% isoflurane for 16 h than that in control cells. The combination of 2% isoflurane and desferrioxamine, a hypoxia mimetic, caused a higher level of HIF-1alpha protein than that induced by 2% isoflurane alone. Reoxygenation and inhibitor of proteasome pathway MG132 did not affect the isoflurane-induced HIF-1alpha protein accumulation. Cycloheximide, an inhibitor for protein synthesis, completely abrogated the induction of HIF-1alpha protein by isoflurane. Isoflurane stimulated heme oxygenase 1, inducible nitric oxide synthase, and VEGF mRNA expression in a concentration-dependent manner, and inactivation of HIF-1alpha attenuated the induction of VEGF mRNA by isoflurane. Conclusion Isoflurane can up-regulate HIF-1alpha and enhance HIF-1-responsive genes heme oxygenase 1, inducible nitric oxide synthase, and VEGF mRNA expression in Hep3B cells. The induction of HIF-1alpha by isoflurane does not involve protein degradation but depends on translation pathway.

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Wakeno-Takahashi, Mayu, Hajime Otani, Shinichi Nakao, Hiroji Imamura, and Koh Shingu. "Isoflurane induces second window of preconditioning through upregulation of inducible nitric oxide synthase in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (2005): H2585—H2591. http://dx.doi.org/10.1152/ajpheart.00400.2005.

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The second window of preconditioning (SWOP) induced by inhalation of volatile anesthetics has been documented in the rat heart and is triggered by nitric oxide synthase (NOS), but involvement of NOS in the mediator phase of isoflurane-induced SWOP has not been demonstrated. We tested the hypothesis that isoflurane-induced SWOP is mediated through upregulation of inducible NOS (iNOS). Rats inhaled 0.75 minimum alveolar concentration (MAC) isoflurane, 1.5 MAC isoflurane, or O2 for 2 h. After 24, 48, 72, and 96 h, the isolated heart was perfused with buffer and subjected to 30 min of ischemia followed by 2 h of reperfusion. Inhalation of 0.75 and 1.5 MAC isoflurane significantly limited infarct size after ischemia-reperfusion 24–72 h after isoflurane inhalation. The maximum effect was obtained 48 h after inhalation of 1.5 MAC isoflurane. Postischemic left ventricular function was improved only 48 h after inhalation of 1.5 MAC isoflurane. iNOS expression and activity in the heart were increased 24–72 h after inhalation of 1.5 MAC isoflurane; this increase was less pronounced after inhalation of 0.75 MAC isoflurane. A selective iNOS inhibitor, 1400W (10 μM), abolished iNOS activation and cardioprotection induced 48 h after inhalation of 1.5 MAC isoflurane. These results suggest that isoflurane inhalation induces SWOP after 24–72 h through overexpression and activation of iNOS in the rat heart.

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Yi, Xiuwen, Yirong Cai, and Wenxian Li. "Isoflurane Damages the Developing Brain of Mice and Induces Subsequent Learning and Memory Deficits through FASL-FAS Signaling." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/315872.

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Background. Isoflurane disrupts brain development of neonatal mice, but its mechanism is unclear. We explored whether isoflurane damaged developing hippocampi through FASL-FAS signaling pathway, which is a well-known pathway of apoptosis.Method. Wild type and FAS- or FASL-gene-knockout mice aged 7 days were exposed to either isoflurane or pure oxygen. We used western blotting to study expressions of caspase-3, FAS (CD95), and FAS ligand (FASL or CD95L) proteins, TUNEL staining to count apoptotic cells in hippocampus, and Morris water maze (MWM) to evaluate learning and memory.Result. Isoflurane increased expression of FAS and FASL proteins in wild type mice. Compared to isoflurane-treated FAS- and FASL-knockout mice, isoflurane-treated wild type mice had higher expression of caspase-3 and more TUNEL-positive hippocampal cells. Expression of caspase-3 in wild isoflurane group, wild control group, FAS/FASL-gene-knockout control group, and FAS/FASL-gene-knockout isoflurane group showed FAS or FASL gene knockout might attenuate increase of caspase-3 caused by isoflurane. MWM showed isoflurane treatment of wild type mice significantly prolonged escape latency and reduced platform crossing times compared with gene-knockout isoflurane-treated groups.Conclusion. Isoflurane induces apoptosis in developing hippocampi of wild type mice but not in FAS- and FASL-knockout mice and damages brain development through FASL-FAS signaling.

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Flood, Pamela, James M. Sonner, Diane Gong, and Kristen M. Coates. "Isoflurane Hyperalgesia Is Modulated by Nicotinic Inhibition." Anesthesiology 97, no. 1 (2002): 192–98. http://dx.doi.org/10.1097/00000542-200207000-00027.

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Background The inhaled anesthetic isoflurane inhibits neuronal nicotinic acetylcholine receptors (nAChRs) at concentrations lower than those used for anesthesia. Isoflurane produces biphasic nociceptive responses, with both hyperalgesia and analgesia within this concentration range. Because nicotinic agonists act as analgesics, the authors hypothesized that inhibition of nicotinic transmission by isoflurane causes hyperalgesia. Methods The authors studied female mice at 6-8 weeks of age. They measured hind paw withdrawal latency at isoflurane concentrations from 0 to 0.98 vol% after the animals had received a nicotinic agonist (nicotine), a nicotinic antagonist (mecamylamine or chlorisondamine), or saline intraperitoneally. In addition, the authors tested the interactions between mecamylamine and isoflurane and nicotine and isoflurane in heterologously expressed alpha(4)beta(2) nAChRs. Results Female mice had significant hyperalgesia from isoflurane. Nicotine administration prevented isoflurane-induced hyperalgesia without altering the antinociception produced by higher isoflurane concentrations. Mecamylamine treatment caused a biphasic nociceptive response similar to that caused by isoflurane. Mecamylamine and isoflurane had an additive effect, both at heterologously expressed alpha(4)beta(2) nAChRs and on the production of hyperalgesia in vivo. Mecamylamine thus potentiated hyperalgesia but did not affect analgesia. Conclusions Since hyperalgesia occurs in vivo at isoflurane doses that antagonize nAChRs in vitro, is prevented by a nicotinic agonist, and is mimicked and potentiated by nicotinic antagonists, the authors conclude that isoflurane inhibition of nAChRs activation is involved in the pathway that causes hyperalgesia. At subanesthetic doses, isoflurane can either enhance pain responses (produce hyperalgesia) or be analgesic (antinociceptive). In rats, low volatile anesthetic concentrations (0.1-0.2 minimum alveolar concentration [MAC]) elicit hyperalgesia, while 0.4-0.6 MAC elicits antinociception.

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