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Journal articles on the topic 'Desfluran'

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Published: 4 June 2021

Last updated: 18 February 2022

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1

Wilhelm, W., M. Kuster, B. Larsen, and R. Larsen. "Desfluran und Isofluran." Der Anaesthesist 45, no. 1 (1996): 37–46. http://dx.doi.org/10.1007/s001010050238.

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2

Baum, J., M. Berghoff, H. G. Stanke, M. Petermeyer, and G. Kalff. "Niedrigflußnarkosen mit Desfluran." Der Anaesthesist 46, no. 4 (1997): 287–93. http://dx.doi.org/10.1007/s001010050403.

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3

Fröba, G. "Alternativen zu Lachgas - Desfluran." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 36, no. 10 (2001): 646–48. http://dx.doi.org/10.1055/s-2001-17679.

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Messmer, M., F. Gerheuser, and H. Forst. "Desfluran bei akute intermittierender Porphyrie." Der Anaesthesist 53, no. 3 (2004): 244–48. http://dx.doi.org/10.1007/s00101-003-0615-7.

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5

Buchinger, H., S. Kreuer, M. Paxian, R. Larsen, and W. Wilhelm. "Desfluran und Isofluran bei Niedrigflussnarkosen." Der Anaesthesist 55, no. 8 (2006): 854–60. http://dx.doi.org/10.1007/s00101-006-1059-7.

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6

Conzen, P. "Sevofluran, Desfluran - und immer noch kein Ende!" Der Anaesthesist 49, no. 10 (2000): 867–68. http://dx.doi.org/10.1007/s001010070038.

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7

Schurig, Volker, Markus Juza, Bernard S. Green, Jörg Horakh, and Arndt Simon. "Die absoluten Konfigurationen der Inhalationsanästhetica Isofluran und Desfluran." Angewandte Chemie 108, no. 15 (1996): 1814–16. http://dx.doi.org/10.1002/ange.19961081524.

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8

Loscar, M., T. Allhoff, E. Ott, P. Conzen, and K. Peter. "Aufwachverhalten und kognitive Funktion nach Desfluran oder Isofluran." Der Anaesthesist 45, no. 2 (1996): 140–45. http://dx.doi.org/10.1007/s001010050248.

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9

KAVRUT ÖZTÜRK, Nilgün, Kaan KATIRCIOĞLU, Murat ÖZKALKANLI, Nuri AYGÜN, and Serdar SAVACI. "QTc Interval During Desflurane Anesthesia: The Effects of Intravenous Lidocaine Prior to Intubation." Turkiye Klinikleri Journal of Medical Sciences 30, no. 4 (2010): 1299–304. http://dx.doi.org/10.5336/medsci.2009-13662.

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10

Navarro, E. "Desfluran-Allgemeinanästhesie zur Sectio caesarea: Vergleich mit Isofluran und Epiduralanästhesie." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 35, no. 04 (2000): 232–36. http://dx.doi.org/10.1055/s-2000-11988.

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11

Byhahn, C., V. Lischke, and K. Westphal. "Arbeitsplatzbelastung im Krankenhaus mit Lachgas und den neuen Inhalationsanästhetika Desfluran und Sevofluran." DMW - Deutsche Medizinische Wochenschrift 124, no. 06 (2008): 137–41. http://dx.doi.org/10.1055/s-2007-1024254.

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M, Şakar. "Yüksek ve Düşük Akımlı Desfluran Anestezisinin Hemodinami, Derlenme ve Maliyet Açısından Karşılaştırılması." Konuralp Tıp Dergisi 2014, no. 2 (2014): 34. http://dx.doi.org/10.18521/ktd.43220.

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13

CÜCE, Neslihan, Alper YOSUNKAYA, Hale BORAZAN, Hasan ESEN, and Said BODUR. "The Relation of Paraoxonase Levels with the Histopathology of the Old Rat Liver Tissue After Repeated Desflurane Anesthesia." Turkiye Klinikleri Journal of Medical Sciences 33, no. 3 (2013): 716–25. http://dx.doi.org/10.5336/medsci.2012-30654.

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14

Karakoç, Ebru, İlkay Ceylan, and Belkıs Tanrıverdi. "Kardiovasküler Cerrahi Anestezisinde Ekstrakorporeal Dolaşımda Sevofluran ve Desfluran Kullanımının BIS Monitorizasyonu ile Değerlendirilmesi." OSMANGAZİ JOURNAL OF MEDICINE 40, no. 3 (2018): 44–52. http://dx.doi.org/10.20515/otd.405497.

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15

Rehberg, B., R. Rüschner, M. Fischer, B. Ebeling, and A. Hoeft. "Konzentrationsabhängige Veränderungen der Latenz und Amplitude somatosensorisch evozierter Potentiale durch Desfluran, Isofluran und Sevofluran." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 33, no. 07 (1998): 425–29. http://dx.doi.org/10.1055/s-2007-994279.

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16

Grundmann, U., A. Risch, S. Kleinschmidt, R. Klatt, and R. Larsen. "Remifentanil-Propofol- Anästhesie bei Bandscheibenoperationen: ein Vergleich mit einer Desfluran-N 2 O- Inhalationsanästhesie." Der Anaesthesist 47, no. 2 (1998): 102–10. http://dx.doi.org/10.1007/s001010050534.

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17

EROL, Atilla, Ruhiye REİSLİ, İsmail REİSLİ, and Şeref OTELCİOĞLU. "The Effects of Sevoflurane, Desflurane and Propofol on the Percentages and Activation Molecules of the Lymphocytes: A Flow Cytometry Analysis of Bronchoalveolar Lavage Fluid." Turkiye Klinikleri Journal of Medical Sciences 31, no. 2 (2011): 443–49. http://dx.doi.org/10.5336/medsci.2008-9364.

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18

Wilhelm, W., K. Berg, A. Langhammer, C. Bauer, A. Biedler, and R. Larsen. "Remifentanil bei gynäkologischen Laparoskopien - Ein Vergleich von Aufwach- und Kreislaufverhalten bei Kombination mit Desfluran oder Propofol." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 33, no. 09 (1998): 552–56. http://dx.doi.org/10.1055/s-2007-994810.

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19

ŞAHİN, Tuna, and Dilek ÖZCENGİZ. "Searching the Effects of Applying Caudal Block or I.V. Tramadol on Bispectral Index, Emergence Agitation and Recovery in Children Under Desflurane Anesthesia." Turkiye Klinikleri Journal of Anesthesiology Reanimation 13, no. 1 (2015): 1–7. http://dx.doi.org/10.5336/anesthe.2014-41656.

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20

Motsch, J., J. Epple, M. Fresenius, S. Neff, W. Schmidt, and E. Martin. "Desfluran versus Isofluran bei geriatrischen Patienten. Ein Vergleich von Aufwachverhalten und postoperativer Befindlichkeit nach abdominal-chirurgischen Eingriffen." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 33, no. 05 (1998): 313–20. http://dx.doi.org/10.1055/s-2007-994255.

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21

Schindler, E., M. Müller, B. Zickmann, H. Kraus, K. H. Reuner, and G. Hempelmann. "Untersuchungen zur Durchblutung der Leber beim Menschen nach 1 MAC Desfluran im Vergleich zu Isofluran und Halothan." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 31, no. 06 (1996): 344–48. http://dx.doi.org/10.1055/s-2007-995933.

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22

Byhahn, Christian, Hans-Joachim Wilke, Ulrich Strouhal, and Klaus Westphal. "Keine Kontamination des ärztlichen Personals mit den Inhalationsanästhetika Desfluran und Lachgas während operativer Eingriffe in der Augenheilkunde." Klinische Monatsblätter für Augenheilkunde 215, no. 12 (1999): 367–69. http://dx.doi.org/10.1055/s-2008-1034734.

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23

Schuster, Frank, and Stephan Johannsen. "Maligne Hyperthermie: pharmakologische Therapie – Update 2019." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 54, no. 09 (2019): 549–58. http://dx.doi.org/10.1055/a-0725-7577.

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ZusammenfassungDie maligne Hyperthermie (MH) ist eine subklinische, autosomal-dominant vererbte, pharmakogenetische Erkrankung der Skelettmuskulatur, die durch alle klinisch eingesetzten volatilen Anästhetika (Sevofluran, Desfluran, Isofluran) und das depolarisierende Muskelrelaxans Succinylcholin bei disponierten Patienten ausgelöst werden kann. Durch die Einführung von Dantrolen konnte die Sterblichkeit von vorher über 80% auf deutlich unter 10% reduziert werden. Zur initialen Therapie einer MH wird ein Bolus von 2,5 mg/kg Dantrolen bezogen auf das tatsächliche Patientengewicht verabreicht.

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24

Bauer, C., Christiane Sattel, U. Grundmann, M. Bauer, I. Marzi, and R. Larsen. "Effekte von Desfluran auf die Lebermikrozirkulation im Vergleich zu Isofluran und Pentobarbital - Eine intravitalmikroskopische Untersuchung an der Ratte." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 30, no. 04 (1995): 226–30. http://dx.doi.org/10.1055/s-2007-996480.

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25

Uçak, Dilek ,., Yasemin Güneş, Ebru Biricik, and Murat Ilgınel. "Altmışbeş yaş üzeri hastalarda tek doz esmolol’ün desfluran ve sevofluran anestezisinde trakeal entübasyona yanıt ve bispektral indeks üzerine etkisi." Cukurova Medical Journal (Çukurova Üniversitesi Tıp Fakültesi Dergisi) 42, no. 4 (2017): 709–15. http://dx.doi.org/10.17826/cutf.325723.

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26

Genç, Selçuk, Hüseyin Bozkurt, Hakan Efe, Temel Deniz Şeren, and Hasan Koçoğlu. "The comparison of the effects of bispectral index controlled minimal, low and high flow desfluran anesthesia on hemodynamics and recovery in patients undergoing lower abdominal surgery." Cumhuriyet Medical Journal 38, no. 2 (2016): 140. http://dx.doi.org/10.7197/cmj.v38i2.5000189957.

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27

Toma, Octavian, Nina C. Weber, Jessica I. Wolter, Detlef Obal, Benedikt Preckel, and Wolfgang Schlack. "Desflurane Preconditioning Induces Time-dependent Activation of Protein Kinase C Epsilon and Extracellular Signal-regulated Kinase 1 and 2 in the Rat Heart In Vivo." Anesthesiology 101, no. 6 (2004): 1372–80. http://dx.doi.org/10.1097/00000542-200412000-00018.

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Background Activation of protein kinase C epsilon (PKC-epsilon) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) are important for cardioprotection by preconditioning. The present study investigated the time dependency of PKC-epsilon and ERK1/2 activation during desflurane-induced preconditioning in the rat heart. Methods Anesthetized rats were subjected to regional myocardial ischemia and reperfusion, and infarct size was measured by triphenyltetrazoliumchloride staining (percentage of area at risk). In three groups, desflurane-induced preconditioning was induced by two 5-min period

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28

Muzi, Michael, Craig W. Lopatka, and Thomas J. Ebert. "Desflurane-mediated Neurocirculatory Activation in Humans." Anesthesiology 84, no. 5 (1996): 1035–42. http://dx.doi.org/10.1097/00000542-199605000-00004.

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Background Rapid increases in the inspired concentration of desflurane have been associated with sympathetic activation, tachycardia, hypertension, and in select cases, myocardial ischemia. The current study examined the effects of the rate of change of the desflurane concentration on the sympathetic and hemodynamic responses to desflurane and sought to determine whether a finite concentration (end-tidal) of desflurane consistently initiated these responses. Methods After Institutional Review Board approval, 23 healthy male volunteers were instrumented for electrocardiogram (heart rate (HR)),

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29

Talke, P., J. Caldwell, B. Dodsont, and C. A. Richardson. "Desflurane and Isoflurane Increase Lumbar Cerebrospinal Fluid Pressure in Normocapnic Patients Undergoing Transsphenoidal Hypophysectomy." Anesthesiology 85, no. 5 (1996): 999–1004. http://dx.doi.org/10.1097/00000542-199611000-00006.

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Background Rapid emergence from anesthesia makes desflurane an attractive choice as an anesthetic for patients having neurosurgery. However, the data on the effect of desflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that isoflurane and desflurane increase intracranial pressure compared with propofol. Methods Anesthesia was induced with intravenous fentanyl and propofol in 30 patients having transsphenoidal hypophysectomy with no evidence of mass effect, and it was maintained with 70% nitrous oxide in oxygen and a continuous 100 microgra

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30

Park, Wyun Kon, Myung Hee Kim, Duck Sun Ahn, et al. "Myocardial Depressant Effects of Desflurane." Anesthesiology 106, no. 5 (2007): 956–66. http://dx.doi.org/10.1097/01.anes.0000265155.01815.6d.

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Background The authors determined whether desflurane altered myocardial excitation-contraction coupling and electrophysiologic behavior in the same manner as isoflurane and sevoflurane. Methods The effects of desflurane on isometric force in guinea pig ventricular papillary muscles were studied in modified standard and in 26 mM K(+) Tyrode solution with 0.1 microm isoproterenol. Desflurane effects on sarcoplasmic reticulum Ca(2+) release were also determined by examining its actions on rat papillary muscles, guinea pig papillary muscles in low-Na(+) Tyrode solution, and rapid cooling contractu

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31

Ebel, Dirk, Jost Müllenheim, Hendrik Südkamp, et al. "Role of Tyrosine Kinase in Desflurane-induced Preconditioning." Anesthesiology 100, no. 3 (2004): 555–61. http://dx.doi.org/10.1097/00000542-200403000-00014.

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Background Short administration of volatile anesthetics preconditions myocardium and protects the heart against the consequences of subsequent ischemia. Activation of tyrosine kinase is implicated in ischemic preconditioning. The authors investigated whether desflurane-induced preconditioning depends on activation of tyrosine kinase. Methods Sixty-four rabbits were instrumented for measurement of left ventricular pressure, cardiac output, and myocardial infarct size (IS). All rabbits were subjected to 30 min of occlusion of a major coronary artery and 2 h of subsequent reperfusion. Rabbits und

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32

Smul, Thorsten M., Markus Lange, Andreas Redel, Natalie Burkhard, Norbert Roewer, and Franz Kehl. "Desflurane-induced Preconditioning against Myocardial Infarction Is Mediated by Nitric Oxide." Anesthesiology 105, no. 4 (2006): 719–25. http://dx.doi.org/10.1097/00000542-200610000-00018.

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Background Volatile anesthetics induce myocardial preconditioning through a signal transduction pathway that is remarkably similar to that observed during ischemic preconditioning. Nitric oxide-dependent signaling plays an important role in anesthetic and ischemic preconditioning. Therefore, the authors tested the hypothesis that desflurane-induced preconditioning is mediated by nitric oxide. Methods Barbiturate-anesthetized rabbits were instrumented for measurement of hemodynamics. All rabbits were subjected to 30-min coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarc

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33

Gueugniaud, Pierre-Yves, Jean-Luc Hanouz, Benoit Vivien, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Effects of Desflurane in Rat Myocardium." Anesthesiology 87, no. 3 (1997): 599–609. http://dx.doi.org/10.1097/00000542-199709000-00021.

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Background The cardiovascular effects of desflurane have been investigated in several in vivo animal and human studies. To determine the possible contributions of myocardial depression, the effects of desflurane on various contractile parameters in isolated cardiac papillary muscles were compared with those of isoflurane and halothane. Methods The effects of desflurane, isoflurane, and halothane (0.5-2.5 minimum alveolar concentration [MAC]) were studied in rat left ventricular papillary muscles (29 degrees C; pH 7.40; stimulation frequency, 12 pulses/min). The inotropic effects were compared

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34

Kojima, Akiko, Yuki Ito, Hirotoshi Kitagawa, Hiroshi Matsuura, and Shuichi Nosaka. "Direct Negative Chronotropic Action of Desflurane on Sinoatrial Node Pacemaker Activity in the Guinea Pig Heart." Anesthesiology 120, no. 6 (2014): 1400–1413. http://dx.doi.org/10.1097/aln.0000000000000165.

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Abstract Background: Desflurane inhalation is associated with sympathetic activation and concomitant increase in heart rate in humans and experimental animals. There is, however, little information concerning the direct effects of desflurane on electrical activity of sinoatrial node pacemaker cells that determines the intrinsic heart rate. Methods: Whole-cell patch-clamp experiments were conducted on guinea pig sinoatrial node pacemaker cells to record spontaneous action potentials and ionic currents contributing to sinoatrial node automaticity, namely, hyperpolarization-activated cation curre

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35

Lenz, Christian, Thomas Frietsch, Carsten Fütterer, et al. "Local Coupling of Cerebral Blood Flow to Cerebral Glucose Metabolism during Inhalational Anesthesia in Rats." Anesthesiology 91, no. 6 (1999): 1720. http://dx.doi.org/10.1097/00000542-199912000-00025.

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Background It is not known whether the effects of desflurane on local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) are different from those of other volatile anesthetics. Methods Using the autoradiographic iodoantipyrine and deoxyglucose methods, LCGU, LCBF, and their overall means were measured in 60 Sprague-Dawley rats (10 groups, n = 6 each) during desflurane and isoflurane anesthesia and in conscious controls. Results During anesthesia, mean cerebral glucose utilization was decreased compared with conscious controls: 1 minimum alveolar concentration (MAC) desflu

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36

Nishimori, C. T., N. Nunes, D. P. Paula, M. L. Rezende, A. P. Souza, and P. S. P. Santos. "Effects of nitrous oxide on minimum alveolar concentration of desflurane in dogs." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 59, no. 1 (2007): 97–104. http://dx.doi.org/10.1590/s0102-09352007000100017.

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Effects of nitrous oxide (N2O) on minimum alveolar concentration (MAC) of desflurane were studied. For that purpose, 30 dogs were randomly allocated into two groups: desflurane group (GD) and N2O and desflurane group (GDN). GD animals received propofol to intubation, and 11.5V% of desflurane diluted in 100% O2. After 30 minutes, they received electric stimulus and if the animal did not react to stimulus, desflurane concentration was reduced by 1.5V%. This protocol was repeated at each 15 minutes, and stimulus was interrupted when voluntary reaction was observed. GDN dogs were submitted to dilu

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37

Lemoine, Sandrine, Lan Zhu, Gallic Beauchef та ін. "Role of 70-kDa Ribosomal Protein S6 Kinase, Nitric Oxide Synthase, Glycogen Synthase Kinase-3β, and Mitochondrial Permeability Transition Pore in Desflurane-induced Postconditioning in Isolated Human Right Atria". Anesthesiology 112, № 6 (2010): 1355–63. http://dx.doi.org/10.1097/aln.0b013e3181d74f39.

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Background Desflurane during early reperfusion has been shown to postcondition human myocardium. Whether it involves "reperfusion injury salvage kinase" pathway remains incompletely studied. The authors tested the involvement of 70-kDa ribosomal protein S6 kinase, nitric oxide synthase, glycogen synthase kinase (GSK)-3beta, and mitochondrial permeability transition pore in desflurane-induced postconditioning. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). After a 30-min

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38

Weiskopf, Richard B., Edmond I. Eger II, Malcolm Daniel, and Mariam Noorani. "Cardiovascular Stimulation Induced by Rapid Increases in Desflurane Concentration in Humans Results from Activation of Tracheopulmonary and Systemic Receptors." Anesthesiology 83, no. 6 (1995): 1173–78. http://dx.doi.org/10.1097/00000542-199512000-00007.

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Abstract Background It was hypothesized that stimulation of rapidly adapting airway receptors produces the transient (2–4 min) circulatory responses to rapid increases in desflurane concentrations greater than 6%. Accordingly, it was reasoned that increasing the concentration of desflurane in one lung, without altering the concentration of desflurane in systemic blood, should cause cardiovascular stimulation, whereas once the airway receptors had adapted to the stimulation, an initial increase in the systemic concentration of desflurane should have little effect.

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Rodig, Gabriele, Cornelius Keyl, Mirko Kaluza, Frieder Kees, and Jonny Hobbhahn. "Effects of Rapid Increases of Desflurane and Sevoflurane to Concentrations of 1.5 MAC on Systemic Vascular Resistance and Catecholamine Response during Cardiopulmonary Bypass." Anesthesiology 87, no. 4 (1997): 801–7. http://dx.doi.org/10.1097/00000542-199710000-00013.

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Background Airway irritation was hypothesized to trigger the transient cardiovascular stimulation associated with desflurane. The authors administered desflurane during cardiopulmonary bypass (CPB), thus avoiding airway contact, and compared the effects of rapid increases of desflurane to 1.5 MAC on systemic vascular resistance index (SVRI) and catecholamine response to those of 1.5 MAC sevoflurane. Methods Forty-eight patients, undergoing elective coronary bypass surgery, were randomly allocated to receive either desflurane or sevoflurane during hypothermic (32-33 degrees C) nonpulsatile CPB

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40

Muzi, Michael, Thomas J. Ebert, William G. Hope, Brian J. Robinson, and Leonard B. Bell. "Site(s) Mediating Sympathetic Activation with Desflurane." Anesthesiology 85, no. 4 (1996): 737–47. http://dx.doi.org/10.1097/00000542-199610000-00008.

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Background Three strategies were employed to better define the afferent site(s) at which desflurane initiates its neurocirculatory activation. Methods Young (aged 19-28 yr) healthy volunteers were employed in three separate studies. Monitoring included electrocardiography, radial artery blood pressure, and direct recordings of sympathetic outflow to skeletal muscle blood vessels by microneurography. In each study, anesthesia was established with 2.5 mg/kg propofol, and in studies 1 and 2 was maintained with 5.4% desflurane via a double-lumen tube. In study 1 (n = 7) a double-lumen tube was pla

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41

Kunst, Gudrun, Astrid G. Stucke, Bernhard M. Graf, Eike Martin, and Rainer H. A. Fink. "Desflurane Induces Only Minor Ca2+Release from the Sarcoplasmic Reticulum of Mammalian Skeletal Muscle." Anesthesiology 93, no. 3 (2000): 832–36. http://dx.doi.org/10.1097/00000542-200009000-00034.

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Background Desflurane is a weaker trigger of malignant hyperthermia than is halothane. There are very few data of the pathophysiologic background of this observation. Therefore, the authors' aim was to investigate the direct effect of desflurane on calcium release in skinned skeletal muscle fibers. Methods For the measurements, single saponin-skinned muscle fiber preparations of BALB/c mice were used. For Ca2+ release experiments, liquid desflurane at 0.6 and 3.5 mm was applied to weakly calcium-buffered solutions with no added Ca2+. Desflurane was diluted in strongly Ca2+-buffered solutions,

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42

Lange, Markus, Andreas Redel, Christopher Lotz та ін. "Desflurane-induced Postconditioning Is Mediated by β-Adrenergic Signaling". Anesthesiology 110, № 3 (2009): 516–28. http://dx.doi.org/10.1097/aln.0b013e318197ff62.

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Background Anesthetic preconditioning is mediated by beta-adrenergic signaling. This study was designed to elucidate the role of beta-adrenergic signaling in desflurane-induced postconditioning. Methods Pentobarbital-anesthetized New Zealand White rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion and were randomly assigned to receive vehicle (control), 1.0 minimum alveolar concentration of desflurane, esmolol (30 mg x kg(-1) x h(-1)) for the initial 30 min of reperfusion or throughout reperfusion, the beta2-adrenergic receptor blocker ICI 118,551 (0.2

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43

Vivien, Benoit, Jean-Luc Hanouz, Pierre-Yves Gueugniaud, Yves Lecarpentier, MD Pierre, and Bruno Riou. "Myocardial Effects of Desflurane in Hamsters with Hypertrophic Cardiomyopathy." Anesthesiology 89, no. 5 (1998): 1191–98. http://dx.doi.org/10.1097/00000542-199811000-00020.

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Background The effects of desflurane on myocardial contraction and relaxation in diseased myocardium have not been completely understood. Methods The effects of desflurane (1.8 to 9.4 vol%) in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C, pH 7.40, Ca2+ 2.5 mM; stimulation frequency, 3/min) under low (isotony) and high (isometry) load. Data are mean percentages of baseline +/- SD. Results Desflurane induced no significant inotropic effect in healthy muscles (maximum unloaded sh

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44

Hanouz, Jean-Luc, Massimo Massetti, Géraldine Guesne, et al. "In Vitro Effects of Desflurane, Sevoflurane, Isoflurane, and Halothane in Isolated Human Right Atria." Anesthesiology 92, no. 1 (2000): 116. http://dx.doi.org/10.1097/00000542-200001000-00022.

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Background Direct myocardial effects of volatile anesthetics have been studied in various animal species in vitro. This study evaluated the effects of equianesthetic concentrations of desflurane, sevoflurane, isoflurane, and halothane on contractile parameters of isolated human atria in vitro. Methods Human right atrial trabeculae, obtained from patients undergoing coronary bypass surgery, were studied in an oxygenated (95% O2-5% CO2) Tyrode's modified solution ([Ca2+]o = 2.0 mM, 30 degrees C, stimulation frequency 0.5 Hz). The effects of equianesthetic concentrations (0.5, 1, 1.5, 2, and 2.5

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Dahan, Albert, Elise Sarton, Maarten van den Elsen, Jack van Kleef, Luc Teppema, and Aad Berkenbosch. "Ventilatory Response to Hypoxia in Humans." Anesthesiology 85, no. 1 (1996): 60–68. http://dx.doi.org/10.1097/00000542-199607000-00009.

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Background At low dose, the halogenated anesthetic agents halothane, isoflurane, and enflurane depress the ventilatory response to isocapnic hypoxia in humans. In the current study, the influence of subanesthetic desflurane (0.1 minimum alveolar concentration [MAC]) on the isocapnic hypoxic ventilatory response was assessed in healthy volunteers during normocapnia and hypercapnia. Methods A single hypoxic ventilatory response was obtained at each of 4 target end-tidal partial pressure of oxygen concentrations: 75, 53, 44, and 38 mmHg, before and during 0.1 MAC desflurane administration. Fourte

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Frost, Katrina, Maaria Shah, Vivian S. Y. Leung, and Daniel S. J. Pang. "Aversion to Desflurane and Isoflurane in Sprague-Dawley Rats (Rattus norvegicus)." Animals 10, no. 6 (2020): 950. http://dx.doi.org/10.3390/ani10060950.

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Carbon dioxide and isoflurane are widely used for killing rats, yet may not truly achieve “euthanasia”, because they elicit aversion. The inhalant anesthetic desflurane is faster acting than isoflurane, representing a potential refinement. Using an aversion-avoidance paradigm, 24 rats were exposed to isoflurane or desflurane (n = 12 per group) at initial exposure. Fourteen rats were then re-exposed to isoflurane or desflurane (n = 7 per group), after a 7 days washout period. Initial exposure: time to recumbency was faster for desflurane than isoflurane (p = 0.0008, 95% CI [-12.9 to 32.6 s]), w

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Rozenberg, Sandrine, Sophie Besse, Julien Amour, Benoît Vivien, Benoît Tavernier, and Bruno Riou. "Effects of Desflurane in Senescent Rat Myocardium." Anesthesiology 105, no. 5 (2006): 961–67. http://dx.doi.org/10.1097/00000542-200611000-00017.

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Background The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness. Methods The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and hig

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Lin, Xue, Ying-nan Ju, Wei Gao, Dong-mei Li, and Chang-chun Guo. "Desflurane Attenuates Ventilator-Induced Lung Injury in Rats with Acute Respiratory Distress Syndrome." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/7507314.

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Ventilator-induced lung injury aggravates the existing lung injury. This study investigated the effect of desflurane on VILI in a rat model of acute respiratory distress syndrome. Forty-eight rats were randomized into a sham (S) group, control (C) group, lipopolysaccharide/ventilation (LV) group, lipopolysaccharide/ventilation/desflurane (LVD) group, or lipopolysaccharide/low ventilation with and without desflurane (LLV and LLVD) groups. Rats in the S group received anesthesia only. Rats in the LV and LVD groups received lipopolysaccharide and were ventilated with a high tidal volume. Rats in

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Ishikawa, Masashi, Masae Iwasaki, Hailin Zhao, et al. "Sevoflurane and Desflurane Exposure Enhanced Cell Proliferation and Migration in Ovarian Cancer Cells via miR-210 and miR-138 Downregulation." International Journal of Molecular Sciences 22, no. 4 (2021): 1826. http://dx.doi.org/10.3390/ijms22041826.

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Inhalational anaesthetics were previously reported to promote ovarian cancer malignancy, but underlying mechanisms remain unclear. The present study aims to investigate the role of sevoflurane- or desflurane-induced microRNA (miRNA) changes on ovarian cancer cell behaviour. The cultured SKOV3 cells were exposed to 3.6% sevoflurane or 10.3% desflurane for 2 h. Expression of miR-138, -210 and -335 was determined with qRT-PCR. Cell proliferation and migration were assessed with wound healing assay, Ki67 staining and Cell Counting Kit-8 (CCK8) assay with or without mimic miR-138/-210 transfections

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Ebert, Thomas J., Francisco Perez, Toni D. Uhrich, and Mark A. Deshur. "Desflurane-mediated Sympathetic Activation Occurs in Humans Despite Preventing Hypotension and Baroreceptor Unloading." Anesthesiology 88, no. 5 (1998): 1227–32. http://dx.doi.org/10.1097/00000542-199805000-00013.

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Background Increasing concentrations of desflurane result in progressive decreases in blood pressure (BP) and, unlike other currently marketed, potent volatile anesthetics, heightened sympathetic nervous system activity. This study aimed to determine whether baroreflex mechanisms are involved in desflurane-mediated sympathetic excitation. Methods Healthy volunteers were anesthetized with desflurane (n = 8) or isoflurane (n = 9). Heart rate (HR; measured by electrocardiograph), blood pressure (BP; measured by arterial catheter), and efferent sympathetic nerve activity (SNA; obtained from percut

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