Disease relevance of C07519

• Somewhat worse azotemia, but comparable tubular necrosis, resulted with desflurane use [1].
• Treatment of refractory status epilepticus with inhalational anesthetic agents isoflurane and desflurane [2].
• Recently, the authors showed that desflurane is a trigger of malignant hyperthermia (MH) in susceptible swine [3].
• The cerebral and systemic hemodynamic and metabolic effects of desflurane-induced hypotension in dogs [4].
• In subjects receiving desflurane, heart rate remained unchanged until the 1.5-MAC level was reached, at which time tachycardia (a 10-beat/min increase) was noted [5].
• Treatment with a combination of 12% desflurane and hypoxia (18% O(2)) (desflurane/hypoxia) for 6 h induced caspase-3 activation, altered APP processing, and increased Abeta generation in H4-APP cells [6].

Psychiatry related information on C07519

• Decreasing anesthetic concentration from 0.75 to 0.25 MAC increased twitch tension by 46 +/- 10% and 25 +/- 7% of control (mean +/- SD, P < 0.001) with desflurane and isoflurane, respectively; 90% response times for these changes were 31 +/- 10 min and 18 +/- 7 min (P < 0.05), respectively [7].
• BACKGROUND: It has recently been demonstrated that the approximately 40-Hz spectral power of the midlatency auditory evoked potential (MLAEP) correlates well with wakefulness during desflurane or propofol anesthesia [8].
• Psychomotor performance after desflurane anesthesia: a comparison with isoflurane [9].
• Analgesia scores were similar for both groups with more amnesia in desflurane group (23% vs 0% P < 0.05) [10].
• Based on these observations, endexpiratory concentrations of > or = 4.5 vol % desflurane should suppress awareness phenomena such as auditory perceptions during anaesthesia [11].

High impact information on C07519

• In eight subjects anesthetized with moderate to high doses of inhalation anesthetics (isoflurane or desflurane) during normocapnia, the onset of electrical silence in EEG was associated with a sudden reduction of blood flow velocity monitored from the middle cerebral artery [12].
• METHODS: Mice were anesthetized with isoflurane or desflurane (fluorinated anesthetics) [13].
• In adult inpatients and outpatients, emergence and orientation are significantly faster after sevoflurane than after isoflurane but not desflurane anaesthesia [14].
• Although further clinical evaluation will define the role of this agent relative to that of propofol and desflurane, sevoflurane should also prove to be a valuable alternative anaesthetic agent for adults in both outpatient and inpatient surgery [14].
• Limited comparative studies with halothane or sevoflurane also suggest an earlier time of emergence from desflurane anaesthesia [15].

Chemical compound and disease context of C07519

• Pressure-flow plots were generated during normoxia and hypoxia on separate days in the conscious state, during sevoflurane (approximately 3.5% end-tidal), and during desflurane (approximately 10.5% end-tidal) anesthesia [16].
• The desflurane group had better neurologic performance (P = 0.023) and greater postoperative weight gain (P = 0.04) than the fentanyl group [17].
• Anesthetized dogs were randomly assigned to increasing concentrations (0.5, 1, and 1.5 times the minimum alveolar concentration) of isoflurane (n = 7) or desflurane (n = 7) in hyperoxia (fraction of inspired oxygen, 0.4) and hypoxia (fraction of inspired oxygen, 0.1) [18].
• During the prebypass period, 5% (10/197) of patients developed ECG ischemia, with no difference between patients who received desflurane, 7% (7/99) or sufentanil, 3% (3/98) (P = 0.3) [19].
• Esmolol did not alter myocardial infarct size (65 +/- 5%) but abolished the protective effects of desflurane and sevoflurane (57 +/- 4 and 52 +/- 4%, respectively) and attenuated ischemic preconditioning (40 +/- 4%) [20].

Biological context of C07519

• Desflurane clinical pharmacokinetics and pharmacodynamics [21].
• Intraoperatively, heart rate greater than 120% of baseline was more common with desflurane; blood pressures were similar for the two anesthetics [22].
• Systolic blood pressure decreased in all but the patients receiving 1.0 MAC desflurane [23].
• The effect of pyrogen administration on sweating and vasoconstriction thresholds during desflurane anesthesia [24].
• Desflurane-induced decreases in systemic vascular resistance occur primarily because of effects on arteriolar resistance vessels [25].

Anatomical context of C07519

• The pharmacodynamic properties of desflurane generally resemble those of isoflurane; thus, it produces dose-dependent depression of the central nervous and cardiorespiratory systems, and tetanic fade at the neuromuscular junction [15].
• Desflurane, a coronary vasodilator, may induce myocardial ischemia in patients with coronary artery disease [19].
• The absence of desflurane-induced intramyocardial catecholamine release was related to hamster myocardium characteristics [26].
• Sympathetic nervous system activation and hyperdynamic circulation associated with desflurane: not all isomers are created equal [27].
• The purpose of this study was to compare the effects of 1 MAC desflurane with those of isoflurane on cerebrospinal fluid pressure (CSFP) in patients with supratentorial mass lesions and a mass effect on computerized tomography (CT scan) [28].

Associations of C07519 with other chemical compounds

• General anesthesia was induced using thiopental and rocuronium and maintained with desflurane, nitrous oxide, and fentanyl or sufentanil [29].
• In vitro, isoflurane, enflurane, or desflurane in oxygen was passed through dried carbon dioxide absorbents at 35, 45, and 55 degrees C. Gases were analyzed by gas chromatography and by mass spectrometry [30].
• The MAC of desflurane in O2 was 7.25 +/- 0.0 (mean +/- SD) in the 18-30-yr age group, and 6.0 +/- 0.29 in the 31-65-yr group; the addition of 60% N2O reduced the MAC to 4.0 +/- 0.29 and 2.83 +/- 0.58, respectively [31].
• In separate groups, the selective blocker esmolol or the protein kinase A inhibitor H-89 (250 microg/kg) was given alone and in combination with desflurane, sevoflurane, and ischemic preconditioning [20].
• A crossover study was performed in volunteers on the ability of desflurane and isoflurane to potentiate the neuromuscular effect of vecuronium, to influence its duration of action, and on the magnitude and time course of reversal of potentiation when anesthesia was withdrawn [7].

Gene context of C07519

• Inhalation of desflurane during endotoxemia showed a significant decrease in release of the proinflammatory cytokines TNF-alpha (-61%, P< or =0.05) and IL-1beta (-47%, P< or =0.05) in plasma as compared to LPS-only group, whereas the release of IL-6 was not significantly affected by desflurane [32].
• RESULTS: Studies with two-electrode voltage clamp at room temperature showed that halothane, isoflurane, and desflurane increased TOK1 outward currents by 48-65% in barium Frog Ringer's perfusate [33].
• Desflurane related ischemia-reperfusion injury reduction correlates well with expression inhibition of ICAM-1, VCAM-1, and E-selectin that mediates neutrophil rotation and firm adhesion on the vascular endothelium [34].
• HUVEC were preconditioned for 60 min with 1 minimum alveolar concentration desflurane before stimulating with TNF-alpha [34].
• Absence of the GluR6 subunit did not change the minimum alveolar concentration of isoflurane, desflurane, or halothane [35].

Analytical, diagnostic and therapeutic context of C07519

• Because it has a high vapour pressure desflurane needs a special delivery system, a heated, pressurised vaporizer [21].
• Desflurane, 3%, in combination with 60% nitrous oxide in oxygen was administered for maintenance of general anesthesia [36].
• However, propofol was associated with a lower incidence of nausea than was desflurane after outpatient anesthesia for laparoscopic surgery [37].
• In the control group, the inspired desflurane concentration was varied based on standard clinical signs [36].
• Desflurane as a marker of limb-to-systemic leak during hyperthermic isolated limb perfusion [38].

References