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Journal articles on the topic 'Isoflurane'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 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

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2

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 an

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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 obtain

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4

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 nativ

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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 anesthet

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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

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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:

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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 suber

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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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10

&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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11

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

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12

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

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13

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

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14

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

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15

&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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17

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

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18

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

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19

&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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21

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

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22

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

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23

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

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24

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

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25

&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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27

&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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30

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

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31

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

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32

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

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33

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

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34

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

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35

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

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36

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

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37

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

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38

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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39

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

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40

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

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41

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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42

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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43

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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44

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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45

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 ox

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46

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. Me

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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

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48

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 fol

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49

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. Isofluran

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50

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 animal

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