Disease relevance of Sevofluran

• Sevoflurane-associated arrhythmias were mainly single supraventricular ectopic beats [1].
• Renal toxicity with sevoflurane: a storm in a teacup [2]?
• Sevoflurane is well tolerated by adult and paediatric patients during induction of anaesthesia, with a low incidence of mild airway complications (breath-holding, coughing, excitement and laryngospasm) [3].
• The pharmacokinetics of sevoflurane do not change in children, obese patients or patients with renal insufficiency [4].
• RESULTS: Preconditioning of trabeculae with sevoflurane preserved contractile function after ischemia [5].

Psychiatry related information on Sevofluran

• CONCLUSIONS: BLA lesions block sevoflurane-induced amnesia [6].
• Sevoflurane and nitrous oxide both impaired psychomotor performance and produced changes in mood [7].
• Based on these observations, > or = 1.5 vol% sevoflurane should suppress phenomena such as auditory perceptions, intraoperative wakefulness, and awareness [8].
• METHODS: We tested the effects of random doses of 0, 0.1, 0.2 and 0.3 MAC sevoflurane in six subjects, in a double-blind study using two measures of behavioural impairment: saccadic latency and stop signal reaction time (SSRT) in a countermanding task [9].
• Dose-related effect of sevoflurane sedation on higher control of eye movements and decision making [9].

High impact information on Sevofluran

• It is suggested that the increase in threshold produced by sevoflurane is due to depression of Na(+) currents at the nodes of Ranvier of corticospinal axons [10].
• Halothane doubled C-fiber responsiveness to capsaicin injected into the left atrium or nebulized to the larynx and to laryngeal hyperinflation, compared with sevoflurane, but it had no effect on baseline activity [11].
• After administration of halothane or sevoflurane to the functionally isolated upper airway, laryngeal C-fiber afferents recorded from the internal branch of the superior laryngeal nerve and identified by a conduction velocity of less than 2.0 m/second were tested for responsiveness to chemical and mechanical stimuli [11].
• We examined the effects of two popular volatile anesthetics, halothane and sevoflurane, on laryngeal C-fiber responsiveness in urethane-anesthetized guinea pigs (from age 4-5 weeks) [11].
• Sevoflurane treatment resulted in phosphorylation of prosurvival kinases, ERK and Akt, and increased de novo HSP-70 protein synthesis without affecting the synthesis of HSP-27 or HSP-32 [12].

Chemical compound and disease context of Sevofluran

• We studied whether sevoflurane, compared with isoflurane, attenuates bronchospasm in dogs [13].
• Propofol, sevoflurane, and HOE 642 also attenuated the onset and magnitude of ischemic contracture and preserved high-energy phosphates (HEPs) compared with controls [14].
• CONCLUSIONS: Both halothane and sevoflurane substantially reduced damage in this focal ischemia model when compared to outcome resulting from the same insult induced in awake rats [15].
• 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%) [16].
• CONCLUSIONS: The reduction in sevoflurane requirements for loss of consciousness and skin incision by fentanyl was determined [17].

Biological context of Sevofluran

• In an alkaline rebreathing circuit, the inhalation anesthetic sevoflurane degrades into at least two products, one of them being the chiral halodiether 1,1,1,3,3-pentafluoro-2-(fluoromethoxy)-3-methoxypropane (halodiether B) [18].
• Clinical pharmacokinetics of sevoflurane [4].
• The relationship between glutamate and dopamine release, apoptosis and ischaemic damage was studied following induction of transient focal cerebral ischaemia under normothermic (37 degrees C) and postischaemic (resuscitative) mild hypothermic (34 degrees C for 2 h) conditions in sevoflurane anaesthetized male Wistar rats [19].
• Sevoflurane reduced necrotic cell death induced with H2O2 in HK-2 cells as well as in LLC-PK1 cells [12].
• RESULTS: Sevoflurane did not alter heart rate or cardiac index at all concentrations compared with awake values [20].

Anatomical context of Sevofluran

• Halothane, isoflurane and sevoflurane reversibly increased NADH fluorescence (autofluorescence) in intact ventricular myocytes of guinea-pig, suggesting that NADH oxidation was impaired [21].
• Halothane, isoflurane and sevoflurane inhibit NADH:ubiquinone oxidoreductase (complex I) of cardiac mitochondria [21].
• We examined the influence of two clinically relevant concentrations (1 and 2 MAC (minimum alveolar concentration)) of halothane and sevoflurane on both efflux and reverse modes of Na+-Ca2+ exchange (NCX) in enzymatically dissociated adult rat cardiac myocytes [22].
• These data suggest a cardioprotective effect of sevoflurane during coronary artery surgery [23].
• It is uncertain to what extent decreases in Ca2+ sensitivity of the contractile proteins play a role in the negative inotropic effect of sevoflurane in intact cardiac muscle tissue [24].

Associations of Sevofluran with other chemical compounds

• This study shows that the halogenated ether anesthetics isoflurane, sevoflurane, and enflurane are also bound to the hydrophobic core of the four-alpha-helix bundle, using isothermal titration calorimetry [25].
• Other recovery parameters (e.g. times to sitting, ambulation) occur at similar times after either sevoflurane or desflurane anaesthesia [3].
• BACKGROUND: During low-flow or closed-circuit anesthesia with the fluorinated inhalation anesthetic sevoflurane, compound A, an olefinic degradation product with known nephrotoxicity in rats, is generated on contact with alkaline CO(2) adsorbents [26].
• At higher concentrations, complete inhibition of action potential activity was observed with sevoflurane but not with propofol [27].
• RESULTS: Remifentanil synergistically decreased the amount of sevoflurane necessary to produce sedation and analgesia [28].

Gene context of Sevofluran

• While almost anesthetics are metabolized by the cytochrome P450 (CYP) 3A4, some major volatile ones such as halothane and sevoflurane are metabolized by CYP2E1 in humans [29].
• Death signaling was not mediated via the Fas/CD95 receptor pathway because neither anti-Fas/CD95 receptor antagonism nor FADD deficiency or caspase-8 deficiency were able to attenuate sevoflurane-mediated apoptosis [30].
• Our data suggest that sevoflurane anaesthesia transiently produced an impaired AQP2 response to an increase in intrinsic AVP [31].
• These data suggest that sevoflurane-produced inhibition of Ang II-induced vasoconstriction is, at least in part, caused by depression of the p44/42 MAPK-mediated signaling pathway [32].
• Sevoflurane-mediated suppression of AP-1 could be observed in primary CD3 lymphocytes from healthy volunteers, was time-dependent and concentration-dependent, and occurred at concentrations that are clinically achieved [33].

Analytical, diagnostic and therapeutic context of Sevofluran

• Fifteen patients undergoing comparable operations with SF (approximately one-half as toxic as IF in vitro) and nine patients undergoing regional/ local anesthesia were controls [34].
• METHODS: Twenty patients (American Society of Anesthesiologists physical status I), aged 20-68 yr undergoing body surface surgery with general anesthesia with sevoflurane were enrolled [35].
• The authors hypothesized that the vaporizer settings required to maintain constant end-expired sevoflurane concentration (Etsevo) during minimal-flow anesthesia (MFA, fresh gas flow of 0.5 l/min) or low-flow anesthesia (LFA, fresh gas flow of 1 l/min) would be lower when sevoflurane is used in oxygen-nitrous oxide than in oxygen [36].
• Influence of nitrous oxide on minimum alveolar concentration of sevoflurane for laryngeal mask insertion in children [37].
• Prediction probability values for EEG parameters and sevoflurane concentration to predict depth of sedation and anesthesia were also calculated [38].

References