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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enflurane can produce seizure activity in the cortical EEG, in vivo, at concentrations associated with surgical anaesthesia. The present study was designed to determine whether this seizure-like burst activity could occur in isolated cortical neurones. Enflurane altered synaptic transmission in the in vitro rat hippocampal slice preparation and produced seizure-like burst discharges of CA 1 neurones, at vapour concentrations equivalent to those obtained during anaesthesia (2-6 vol%; 0.5-1.5 mmol litre-1). Burst discharges occurred both spontaneously and in response to stimulation of stratum radiatum fibres in the CA 1 pyramidal region, but not in the dentate area. Low concentrations of enflurane (approx. 0.75 mmol litre-1), decreased the field potential responses of CA 1 neurones; however, dentate granule neurone responses were increased. Input/output analyses of field excitatory post-synaptic potential (EPSP) and population spike amplitudes revealed that the enflurane-induced depression of field potential responses was associated with decreases in synaptic input, whereas burst activity resulted from a decrease in the threshold of CA 1 neurones.
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PMID:Enflurane-induced burst firing of hippocampal CA 1 neurones. In vitro studies using a brain slice preparation. 382 86

Ten patients for coronary vein grafting had induction of anesthesia with fentanyl (30 micrograms/kg), followed by enflurane-oxygen sufficient to decrease systolic blood pressure by 27% before intubation. Enflurane was continued in concentrations to maintain blood pressure below that with patients awake. All patients had preserved ventricular function and effective beta-blockade. Studies of hemodynamic functions and myocardial blood flow and oxygenation were done before induction, six times during anesthesia, and twice postoperatively. The blood pressure decrease on induction and before bypass was due to reduced cardiac index without decreased heart rate or systemic resistance. Stroke work index decreased 47% on induction and remained below awake level throughout. Coronary sinus blood flow decreased 26% after intubation and remained so before bypass. Without change in coronary resistance, coronary sinus oxygen content increased 30% on induction and stayed elevated before bypass. Normal lactate extraction continued after induction and increased before bypass; mean extraction decreased after bypass, with one or two hearts producing lactate in the first 24 postoperative hr. Fentanyl-enflurane-oxygen maintained a steady mild hemodynamic depression during the operation and soon afterward, which preserved myocardial oxygenation.
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PMID:Myocardial metabolism and hemodynamic responses with fentanyl-enflurane anesthesia for coronary arterial surgery. 394 Apr 69

Enflurane and isoflurane, widely used general anesthetic agents, were shown to significantly inhibit the microbicidal oxidative activity of pulmonary alveolar macrophages (PAM) at clinically relevant concentrations. This inhibition was reversible, as exposing the anesthetic-treated PAM to air for 30 min completely removed any depression of oxidative activity. Using chemoluminigenic probes to analyze the generation of oxidative metabolites, a significant reduction in superoxide anion (O-2) production was found in PAM exposed to enflurane or isoflurane.
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PMID:Enflurane and isoflurane inhibit the oxidative activity of pulmonary alveolar macrophages. 397 91

The physical and pharmacological properties of the structural isomers isoflurane and enflurane differ from each other and from those of other potent inhaled anaesthetics. The minimum alveolar concentration (MAC) for isoflurane (1.15%) is one-and-one-half times that for halothane (0.75%) and two-thirds that for enflurane (1.7%). The blood/gas partition coefficient (1.4) for isoflurane is lower than the coefficients for all other potent inhaled agents. Despite this lower blood solubility, induction of anaesthesia is slightly faster with halothane because of isoflurane's mild pungency. Enflurane depresses ventilation more than isoflurane, which in turn is slightly more depressant than halothane. All these agents dilate constricted bronchi, and thus are useful in the anaesthetic management of patients who have asthma or chronic obstructive pulmonary disease. Isoflurane has the largest circulatory margin of safety of all potent halogenated agents; it produces the least myocardial depression at a given multiple of MAC. Isoflurane may increase heart rate, particularly in younger patients, and occasionally is associated with tachycardia. It decreases total peripheral resistance, thereby decreasing systemic arterial pressure. Although results from one study suggest that isoflurane may produce a "steal" or coronary blood flow in patients with coronary artery disease, results from other studies suggest that, even in the presence of coronary artery disease, coronary blood flow to all parts of the heart remains as adequate with isoflurane as with other anaesthetics. Greater concentrations of isoflurane (1.6 MAC) increase cerebral blood flow less than does halothane. Isoflurane does not produce convulsive activity, but can produce profound muscle relaxation. It enhances the action of tubocurarine or pancuronium, and (to a lesser extent) vecuronium or atracurium. The enhancement is comparable to that produced by enflurane. Less enhancement is produced by halothane or nitrous oxide-narcotic. Only 0.17% of isoflurane taken up in man appears as urinary metabolites. This resistance to biodegradation may explain the minimal or absent hepatotoxicity and nephrotoxicity of isoflurane.
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PMID:The pharmacology of isoflurane. 639 30

The effect of enflurane (2% and 4% inspired) on left ventricular (LV) function were examined in chronically instrumented dogs, both intact and after isolation of their hearts and lungs from the systemic circulation. Enflurane in the intact dogs increased heart rate (32 +/- 5% with 2% and 41 +/- 4% with 4%) and elicited striking, dose-dependent decreases in LV stroke shortening (-30 +/- 3% and -41 +/- 4%), the maximum velocity of LV fiber shortening, dD/dt, (-23 +/- 2%) and -40 +/- 2%), LV systolic pressure (-25 +/- 3% and -33 +/- 2%), the maximum rise of LV-pressure, dP/dt (-33 +/- 5% and -55 +/- 3%), and mean aortic pressure (-27 +/- 2% and -37 +/- 1%). However, the LV diastolic performance was impaired little, i.e., even with the higher concentration the LV end-diastolic pressure rose only moderately (32 +/- 4%), while the LV end-diastolic dimensions failed to change significantly; both LV end-diastolic pressure and LV end-diastolic diameter were decreased with the low concentration. Enflurane, after beta-adrenergic blockade alone or after combined beta-adrenergic and cholinergic blockades, or with spontaneous ventilation instead of controlled ventilation, had similar effects. By contrast, in the hearts that were isolated from the systemic circulation and the complex neurohumoral environment, enflurane increased both LV end-diastolic pressure (116 +/- 32% and 492 +/- 58%) and LV end-diastolic diameter (13 +/- 3% and 28 +/- 7%). In intact dogs with aortic pressure artificially increased to conscious control levels, enflurane likewise caused a distinct depression of the LV diastolic performance. Thus, LV systolic unloading appears to be mandatory in order to prevent acute myocardial failure from higher doses of enflurane. The observed changes in LV function with enflurane are largely independent of cardiac rate, adrenergic and cholinergic influences, and the hemodynamic consequences of intermittent positive-pressure ventilation.
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PMID:Importance of myocardial loading conditions in determining the effects of enflurane on left ventricular function in the intact and isolated canine heart. 682 70

The effects of enflurane and halothane on contractile force of the right ventricle were compared using the Walton-Brodie strain gage arch and pulmonary artery catheter data in dogs anesthetized with pentobarbital. Twenty mongrel dogs were studied to determine the effects of the two anesthetics on contractile force during a 30-minute exposure to four approximate multiples of MAC: 0.75, 1.0, 1.25, and 2.0, and during a 2-h exposure to 1.0 MAC of each agent. Both anesthetics caused a dose-dependent reduction in contractile force, cardiac output, and mean arterial blood pressure. Enflurane caused greater depression of all variables at all concentrations tested. After a 30-min exposure to 0.75, 1.0, 1.25, and 2.0 MAC, halothane depressed contractile force 33.9%, 37.9%, 46.1%, and 73.4%, respectively, and enflurane depressed contractile force 48.4%, 53.5%, 66.6%, and 81.3%, respectively. The depression produced by enflurane at 1.0 and 1.25 MAC was significantly greater (P less than 0.05) than the depression produced by halothane at equal MAC. The reduction of cardiac output by enflurane at 1.25 and 2.0 MAC was significantly greater than that observed with halothane (P less than 0.05). The decrease in mean blood pressure produced by enflurane was significantly greater (P less than 0.05) than the decrease produced by halothane at 1.0, 1.25, and 2.0 MAC. No significant differences between groups were found in temperature, arterial PCO2, PO2, pH, or hematocrit levels. No diminution of the differences in effect on contractility between the two agents was observed when the exposure period was lengthened to two hours at 1.0 MAC.
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PMID:Effects of halothane and enflurane on right ventricular performance in hearts of dogs anesthetized with pentobarbital sodium. 684 18

Enflurance, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20 C). The [Ca2+]--tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10 per cent decrease at 5 per cent enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85 per cent decrease at 2.5-7.5 per cent enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5 per cent), but was decreased at high concentration (25 per cent decrease at 7.5 per cent enflurane). Enflurane (1-7.5 per cent), however, increased (13-44 per cent) the submaximum caffeine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.
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PMID:Effects of enflurane on functionally skinned myocardial fibers from rabbits. 737 71

Enflurane, a new volatile anesthetic agent, was compared with halothane as components of a commonly used clinical anesthetic regime in the pony. Enflurane provides satisfactory general anesthesia when administered at a maintenance concentration of approximately 1.5-2.5%, in combination with a 1:1 nitrous oxide-oxygen mixture. With both agents cardiac rhythm and pulse were stable, however significant arterial hypotension occurred, especially during and following induction, being anesthetic concentration dependent. Hypoventilation was induced by both agents, there being no significant quantitative difference in respiratory depression despite significantly lower respiratory rates with enflurane. Serum electrolytes and liver enzymes did not change significantly with either regime. Emergence from anesthesia was smooth, and significantly more rapid with enflurance. Post-anesthetic complications were not observed with either agent.
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PMID:Enflurane anesthesia in the pony: a comparative study between enflurane and halothane. 737 54

Enflurane anesthesia for cesarean section has given favourable results with regard to anesthetic effect and lack of depression of the neonate. Enflurane is metabolized to fluoride. High serum levels of inorganic fluoride are nephrotoxic. The nephrotoxic level is known for healthy adult kidneys but not for neonatal kidneys. In a study on enflurane anesthesia for cesarean section serum analyses revealed increased inorganic fluoride levels in the neonates. To exclude unwanted effects on the children, a follow-up study was undertaken 6-12 months after delivery. General development and renal function were studied. No abnormalities were found, indicating that enflurane anesthesia for cesarean section has no persistent unfavourable effects on the children.
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PMID:Anesthesia for cesarean section.--VI Late effects on the infant of enflurane anesthesia for cesarean section. 744 35

This is a brief review of some of the salient clinical features of halothane and enflurane, the two most widely used volatile anesthetics in clinical practice today. Although, halothane has an excellent safety record and comes close to being the ideal inhalational anesthetic it does have some undesirable effects, including incompatibility with adrenaline and the possibility of causing disturbed hepatic function when given repeatedly. Enflurane is now established as a satisfactory volatile anesthetic which has considerably less metabolic breakdown than many other agents; if this is reflected in terms of minimal organ toxicity it should continue to have considerable clinical value. The risks of damage to the kidney and cerebral irritability are uncommon but undesirable features of enflurane. In the search of the perfect inhalational anesthetic the most promising compounds will be those with least biotransformation, suitable pharmacokinetics with minimal cardiovascular or respiratory depression and without toxic effects on the liver, kidney or foetus.
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PMID:Clinical features of halothane and enflurane. 745 51


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