Disease relevance of enflurane

• A 57-yr-old female with no previous history of liver disease was exposed to enflurane during three separate surgeries over a 12-mo period [1].
• To study the impact of prolonged inotropic stimulation on the development of myocardial hibernation, the left anterior descending coronary artery was cannulated and hypoperfused at constant flow in 12 enflurane-anesthetized swine [2].
• METHODS: A total of 62 enflurane-anesthetized pigs underwent a protocol of 90-min low-flow ischemia and 120-min reperfusion [3].
• When halothane or enflurane were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was not sustained [4].
• Commonly used surgical levels of enflurane general anesthesia do not cause hypoxia of the inner retina in cats breathing 21% inspired oxygen [5].

Psychiatry related information on enflurane

• Alteration by enflurane of Electrophysiologic correlates of search in short-term memory [6].
• Psychomotor performances remained significantly (P less than 0.05 to P less than 0.001) worse than in an unanesthetized control group for 5 hours after both halothane and enflurane [7].
• Effect of enflurane on cerebellar cGMP and on motor activity in the mouse [8].
• Our results indicate that subanesthetic but not trace levels of enflurane or halothane can impair mental performance and manual dexterity and produce amnesia [9].
• Effects of low concentrations of enflurane on probability learning [10].

High impact information on enflurane

• Halothane (I), enflurane (II), and isoflurane (III), which are among the most important inhalation anesthetics, are currently administered as racemic mixtures [11].
• Thirty-two enflurane/N2O-anesthetized open-chest dogs were subjected to 15 minutes of occlusion of the left circumflex coronary artery (LCx) and 4 hours of subsequent reperfusion [12].
• It was found that halothane and enflurane decreased the transition temperature and increased the width of the transition without affecting the enthalpy change for the main gel-to-liquid crystalline transition [13].
• In oocytes expressing mouse mRNA, enflurane at an anesthetic concentration (1.8 mM) inhibited the NMDA-, AMPA-, and kainate-induced currents by 29-40%, 30-33%, and 20-27%, respectively, suggesting that all three glutamate ionotropic receptors are susceptible to suppression by inhalational anesthetics [14].
• Effects of enflurane, an inhalational anesthetic, on NMDA, AMPA, and kainate-gated currents were examined in Xenopus laevis oocytes expressing mouse or human brain mRNA [14].

Chemical compound and disease context of enflurane

• These findings suggested a greater margin of safety for isoflurane, especially with respect to the heart, and a greater potential for respiratory depression for enflurane than for the other agents [15].
• Patients and rats with chronic renal insufficiency (CRI) anesthetized with enflurane do not have significantly greater increases in postoperative serum inorganic fluoride levels when compared with subjects with normal renal function [16].
• The authors conclude that ketamine, as compared with enflurane, diminishes or prevents arteriolar constriction and tissue hypoxia in the cremaster muscle of hemorrhaged rats [17].
• The authors examined the effects of nifedipine, a sarcolemmal slow Ca2+ channel blocker, on dynamic stiffness and force of rabbit right ventricular trabeculum and papillary muscle in Ba2+ contracture, in an attempt to reproduce the effects of halothane, enflurane, and isoflurane on a similar preparation as reported by Shibata et al [18].
• Thus, neither sevoflurane nor enflurane deteriorated postoperative renal function in these patients with preexisting renal insufficiency [19].

Biological context of enflurane

• Fluoride kinetics after enflurane anesthesia in healthy and anephric patients and in patients with poor renal function [20].
• At the subcortical level, isoflurane and enflurane increased significantly the N13 peak latency and decreased the interval between the N13 peak and P14 peak, which implicates interference with synaptic transmission at the spinal level [21].
• Modulation of the inositol 1,4,5-trisphosphate (IP3)-mediated signal transduction pathway by the inhalational anesthetic enflurane was studied in Xenopus oocytes expressing mouse and human cortical mRNA [22].
• This may be the result of preservation of retinal vascular autoregulation under enflurane anesthesia, retinal vasodilatation secondary to a direct smooth muscle relaxing effect of enflurane, or decreased retinal oxygen use under enflurane anesthesia [5].
• Heart rate response to nociceptive stimulation as an index of anesthetic potency for enflurane [23].

Anatomical context of enflurane

• Hydrophilic region of lecithin membranes studied by bromothymol blue and effects of an inhalation anesthetic, enflurane [24].
• Metabolism of the volatile anesthetic enflurane to inorganic fluoride ion by human liver microsomes in vitro is catalyzed predominantly by the cytochrome P450 isoform CYP2E1 [25].
• In rats anaesthetised with enflurane, we examined the responses of convergent neurones in the dorsal horn of the spinal cord to noxious thermal and mechanical stimulation and to innocuous brushing, during reperfusion of their receptive fields on the tail, following transient ischaemia [26].
• To study the afterload dependence of regional wall excursion in short-term hibernating myocardium, in 11 enflurane-anesthetized swine the left anterior descending coronary artery was cannulated and hypoperfused for 90 min to reduce anterior systolic wall thickening (WT, sonomicrometry) by 60% [27].
• In vitro in mouse microsomes, halothane, enflurane and isoflurane were all inhibitors of aminopyrine metabolism [28].

Associations of enflurane with other chemical compounds

• Correlations were also obtained for five inhalation anesthetics (enflurane, sevoflurane, desflurane, methoxyflurane, and isoflurane) for both in vivo and in vitro metabolism by humans: In[F(-)]peak plasma = 42.87 - 1.57(delta Hact), r2 = 0.86 [29].
• The partial pressures of diethylether, enflurane, and methoxyflurane that decreased the surface potential by 10 mV were 2.1 X 10(-2), 1.7 X 10(-2), and 0.17 X 10(-2) bar, respectively, which were in agreement with the minimal alveolar concentrations of these anesthetics to achieve surgical anesthesia [30].
• The DeltaS degrees values accompanying isoflurane, sevoflurane, and enflurane binding were -8.5 cal/mol K, -10.4 cal/mol K, and -8.0 cal/mol K, respectively [31].
• Potentiation of GABA-activated currents by enflurane was dependent on the composition of GABAA receptor protein subunits; the order of sensitivity was alpha 1 beta 1 > alpha 1 beta 1 gamma 2S = alpha 1 beta 1 gamma 2L > total mRNA [32].
• Recovery room (RR) admission temperatures were similar for the three groups: fentanyl, 36.1 +/- 0.1 degrees C; enflurane, 35.7 +/- 0.2 degrees C; and halothane, 36.0 +/- 0.1 degrees C (P greater than 0.05) [33].

Gene context of enflurane

• RESULTS: Halothane, isoflurane, and enflurane (1 minimum alveolar concentration [MAC], 4 h) decreased rmIL-1beta-stimulated AT II cell secretions of interleukin-6, MIP-2, and MCP-1, but did not modify total protein secretion [34].
• Acute and chronic isoflurane anaesthesia diminished BuChE activity by 70-90% in whole brain instead cerebellum and hippocampus mAChR levels were only altered by chronic enflurane anaesthesia [35].
• These results suggest that P450 2E1 is the predominant P450 isoform responsible for human clinical enflurane metabolism in vivo [25].
• 1. In the present study the mechanisms were examined by which the neuropeptide galanin modulates the extracellular concentrations of striatal acetylcholine (ACh) in enflurane anaesthetized and in freely moving male rats by use of in vivo microdialysis and high performance liquid chromatography [36].
• We have examined the activity of choline acetyltransferase (ChAT) in rat cortical synaptosomes in the presence of three volatile anaesthetic agents: enflurane, halothane and isoflurane [37].

Analytical, diagnostic and therapeutic context of enflurane

• Blood enflurane concentrations were measured by gas chromatography [25].
• Under normoxic conditions, inner retinal oxygen tension remained unchanged or increased slightly as ocular perfusion pressure decreased with deeper levels of enflurane anesthesia [5].
• METHODS AND RESULTS: In 42 enflurane-anesthetized pigs, the LAD coronary artery was cannulated, and subendocardial blood flow (ENDO, microspheres, ml/min/g) and IS (%, TTC-staining) were determined [38].
• Polarographic oxygen microelectrodes were used to measure inner retinal oxygen tension in cats under enflurane anesthesia at 21% inspired oxygen tension [5].
• The nature of the EEG changes at this time was agent-specific (P less than 0.05 by chi-square), with high-frequency changes evident in the enflurane group and shifts in amplitude in the 8-12 Hz activity predominating in the nitrous oxide-enflurane group [39].

References