Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sevoflurane is an halogenated methyl isopropyl ether. It is potent, non explosive and non flammable. It reacts with soda lime to form traces of a related ether which has not been shown to have any toxic effect on animals chronically exposed to it in a closed system. Induction of anaesthesia with sevoflurane is rapid and smooth, as predicted by a blood/gas partition coefficient of about 0.6 and an acceptable odour which allows the use of concentrations of up to 10%. Its MAC has been reported to vary between 1.7 and 2.3 vol %. Sevoflurane causes dose-dependent cardiovascular and respiratory depression. Its effect on the cerebral circulation is similar to that of isoflurane. The extent of biotransformation is similar to that of enflurane, but its low solubility and rapid elimination confine this to the period of inhalation. No toxic effects on the kidneys, liver and haematopoietic system have been found. Desflurane is a fluorinated methyl ether, structurally very similar to isoflurane. It is non flammable and non explosive at clinical concentrations. It is more stable in the presence of soda lime than any of the volatile anaesthetic agents available. This agent must be delivered with a thermostated vaporizer within a closed circle system, as its boiling point is 23.5 degrees C. Desflurane is less potent than isoflurane. Its MAC has been estimated to be about 7.2 vol % in man. Desflurane did not lead to any liver, lung or kidney injury in laboratory rats, even during hypoxia and enzyme induction. Desflurane undergoes little biotransformation, although the presence of volatile metabolites or covalent tissue-bound products cannot be excluded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Desflurane (I 653) and sevoflurane: halogenated anesthetics of the future?]. 144 16

Sevoflurane and desflurane are volatile inhaled anesthetics that are currently being investigated as possible improvements for the anesthetic management of human patients. Information to date suggests these agents have several advantages over existing clinical agents. For example, the blood/gas partition coefficient for both agents is lower than that of other halogenated anesthetics. Consistent with this physical characteristic is a more rapid induction of and emergence from anesthesia. Both cause a dose-related depression of cardiopulmonary function, which is comparable to isoflurane. Results of studies to date favor desflurane over sevoflurane because it is less soluble in blood, is stable in soda lime, is biodegraded the least of any volatile anesthetic, and is not toxic.
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PMID:Other new and potentially useful inhalational anesthetics. 158 70

At present, the most widely used inhalational anaesthetics are the halogenated, inflammable vapours halothane, enflurane, isoflurane and the gas nitrous oxide. The anaesthetic effect of these agents is related to their tension or partial pressure in the brain, represented at equilibrium by the alveolar concentration. The minimum alveolar concentration for a specific agent is remarkably constant between individuals. The uptake and distribution of inhalational anaesthetics depends on inhaled concentration, pulmonary ventilation, solubility in blood, cardiac output and tissue uptake. Inhalational anaesthetics are mainly eliminated by pulmonary exhalation, but significant amounts of halothane are removed by hepatic metabolism. Inhalational agents currently in use have acceptable pharmacokinetic characteristics, and clinical acceptance depends on their potential for adverse effects. Induction of anaesthesia with halothane is rapid and relatively pleasant and it is the agent of choice for paediatric anaesthesia. Between 20 and 50% is metabolised, and the parent drug is a potent inhibitor of drug metabolism. Post-operatively enzyme induction may follow. The major disadvantages of halothane are myocardial depression, propensity to evoke cardiac arrhythmias and the rare but serious halothane hepatitis. Induction and recovery from enflurane anaesthesia is rapid. Metabolism accounts for 5 to 9% of the elimination. The metabolic product inorganic fluoride may in rare cases cause renal toxicity. Enflurane is a weak inhibitor of drug metabolism at anaesthetic concentrations. Enflurane depresses circulation more than halothane by reducing both myocardial contractility and systemic vascular resistance, but cardiac rhythm is stable. Enflurane anaesthesia may, unlike the other agents, induce epileptic activity. Enflurane is widely used as replacement for halothane in adults. Despite its low blood-gas solubility, the airway irritability of isoflurane precludes a faster induction of anaesthesia than with halothane. Isoflurane is almost resistant to biodegradation. Myocardial contractility is maintained during isoflurane anaesthesia and cardiac rhythm is stable except for the occurrence of tachycardia in some patients. Isoflurane is the inhalational agent of choice for neurosurgical operations. Sevoflurane is an experimental ether vapour: induction and recovery is fast and pleasant. It is metabolised to the same extent as enflurane and subnephrotoxic concentrations of inorganic fluoride may result. Sevoflurane has fewer respiratory and cardiovascular depressant effects than halothane and may be a future alternative for paediatric anaesthesia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of the inhalational anaesthetics. 355 39

Increased duration of anaesthetic administration has implications for recovery from anaesthesia, has cardiovascular effects, and potential for toxicity through metabolism and breakdown of the anaesthetics. Recovery of function after desflurane or sevoflurane anaesthesia, because of the low blood gas and tissue solubilities of these agents, is more rapid than after halothane, isoflurane or enflurane, with recovery being most rapid after desflurane. Increased duration of anaesthesia amplifies the differences in rate of recovery because of the additional anaesthetic (greater with more soluble agents) dissolved in tissues. Increased duration of anaesthesia lessens the cardiovascular depression associated with most halogenated inhaled anaesthetics including desflurane, but not isoflurane. Increased duration of anaesthesia allows for greater metabolism of anaesthetics and greater exposure to metabolites and potentially toxic breakdown products. Desflurane is the least metabolised of the available anaesthetics and is stable in soda lime and Baralyme. Thus, it has exceedingly low potential for toxicity. Sevoflurane undergoes considerable metabolism, producing free fluoride ion, with plasma concentrations proportional to dose and duration of anaesthesia exceeding 50 microM in approximately 7% of patients. In rats, the effects of a toxic breakdown product of sevoflurane, CF2 = C(CF3)OCH2F (compound A), are also dose- and duration-dependent, with lower concentrations producing toxic effects as duration of exposure increases. The clinical importance of the metabolism and in vitro breakdown of sevoflurane has still to be adequately tested.
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PMID:Implications of chemical and physical properties of desflurane for longer surgery. 748 20

Sevoflurane is well known to cause depression of cardiovascular function, but detailed information on its actions on the contractility and reactivity of blood vessels is lacking. We have assessed therefore the direct effect of this anaesthetic on the functional reactivity of isolated rabbit mesenteric artery ring preparations. We found that contractions of endothelium intact rings induced by noradrenaline and phenylephrine were significantly attenuated by 4% sevoflurane; the observation that the maximal tension generation decreased without a significant reduction in pD2 is consistent with the view that receptor dysfunction was not involved. The effect of sevoflurane was not affected by NG-monomethyl-L-arginine. Sevoflurane 4% also produced attenuation of noradrenaline-induced contractions of endothelium denuded ring preparations. The contractions of endothelium denuded ring preparations produced by noradrenaline in Ca(2+)-free media in the presence of K+ were not affected by 4% sevoflurane, but sevoflurane depressed external Ca(2+)-dependent contractions. When vasodilators (acetylcholine and nitroglycerin) were added to the bathing media in the presence of 2% sevoflurane, the endothelium-dependent relaxation produced by acetylcholine, but not the endothelium-independent relaxation produced by nitroglycerin, was attenuated; superoxide dismutase inhibited the effect of sevoflurane on endothelium-dependent relaxation. These results are consistent with the view that sevoflurane inhibits alpha adrenoceptor-mediated contractions of isolated rabbit mesenteric artery ring preparations; this effect may be caused by reduced Ca2+ influx, as estimated from the effect on external Ca(2+)-dependent contractions, but is unlikely to be caused by reduced Ca2+ release from the sarcoplasmic reticulum of vascular smooth muscle, as estimated from noradrenaline-induced contractions in Ca(2+)-free bathing media.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of sevoflurane on the vascular reactivity of rabbit mesenteric artery. 777 35

The effects of sevoflurane on contraction and membrane potentials were studied in isolated canine ventricular muscle strips. Sevoflurane depressed electrically-induced contraction in a dose-dependent manner. The inhibitory effect was more pronounced in high-K+ Tyrode solution than in normal Tyrode solution suggesting that sevoflurane inhibits transmembrane Ca2+ influx. In electrophysiological studies, sevoflurane depressed both overshoot and the plateau phase of action potentials. Resting membrane potential was not affected by sevoflurane. We conclude that the depression of myocardial contractility by sevoflurane may be due to block of transmembrane calcium influx.
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PMID:[Effect of sevoflurane on contraction and membrane potentials in canine right ventricular myocytes]. 825 76

Hemodynamic changes and left ventricular performance were investigated by simplified mechanocardiography using finger plethysmography instead of carotid artery pulse tracing in patients who received 4 volatile anesthetics with or without nitrous oxide. Systolic blood pressure (Ps), diastolic blood pressure (Pd), heart rate (HR), pre-ejection period (PEP), left ventricular ejection time (LVET), isovolemic contraction time (ICP), PEP/LVET, Pd/ICT, and 1/PEP2 were selected as indices which represent hemodynamics and systolic time intervals. Enflurane 0.6 and 1.2MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT significantly. Addition of nitrous oxide caused more depression. Halothane 0.6MAC prolonged PEP, and shortened 1/PEP2 and Pd/ICT. Sevoflurane 1.2MAC shortened only 1/PEP2. Addition of nitrous oxide prolonged PEP and PEP/LVET, and shortened Pd/ICT. Isoflurane 1.2MAC lowered Ps and increased HR. The results indicate that cardiac performance was depressed by volatile anesthetics in the order of enflurane, halothane, sevoflurane and isoflurane.
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PMID:[Volatile anesthetics suppress cardiac function in man; an investigation based on systolic time intervals]. 843 99

We studied the effects of sevoflurane on contraction and membrane potentials in isolated canine ventricular muscle strips. Sevoflurane (> 0.5%) depressed electrically induced contraction in a dose-dependent manner. Moreover, sevoflurane did not show stimulation frequency-dependent depression in contraction as shown with local anesthetics. The inhibitory effect was more pronounced in high-K+ Tyrode's solution than in normal Tyrode's solution, suggesting that sevoflurane may inhibit transmembrane Ca2+ influx. In contrast, isoflurane and halothane were equally effective in depressing electrically induced contractions in normal and high-K+ Tyrode's solution. In electrophysiologic experiments, sevoflurane at higher concentrations (> 2.0%) depressed both overshoot and the plateau phase of the action potentials. These depressant effects were more pronounced in high-K+ Tyrode's solution. Resting membrane potential was not affected by sevoflurane. We conclude that depression of myocardial contractility by sevoflurane may be due to a block of the transmembrane calcium influx.
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PMID:Effects of sevoflurane, isoflurane, and halothane on mechanical and electrophysiologic properties of canine myocardium. 849 73

We examined, in guinea pig papillary muscles, whether the negative inotropic effect of sevoflurane is due to the depression of the influx of extracellular Ca2+ or to inhibition of the availability of intracellularly stored Ca2+. Sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normally polarized guinea pig papillary muscles. Sevoflurane produced a depression of contractile force with different rates or patterns of stimulation in the rested state and at low stimulation frequencies. In a potentiated state, sevoflurane did not depress contractile forces. Although sevoflurane decreased action potential duration and contractile force in a concentration-dependent fashion in normal Tyrode's solution, in high K+ Tyrode's solution, it caused a depression of contractile force without a shortening of action potential duration. Sevoflurane also depressed contractile force in normal and high K+ Tyrode's solution with ryanodine 1 microM. Our results suggest that in myocardial contractile force the negative inotropic effect of sevoflurane might be caused by depression of transsarcolemmal Ca2+ influx, accompanied by shortening of the action potential duration.
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PMID:The effects of sevoflurane on contractile and electrophysiologic properties in isolated guinea pig papillary muscles. 862 48

We have assessed the deleterious effects of methylmethacrylate (MMA) on cardiac function and metabolism in the isolated heart-lung preparation with or without volatile anesthetics. Wistar rats were prepared for the heart-lung model. They were randomly divided into 5 groups as follows. (1) Control (C) group. (2) Cement (M) group; they received MMA. (3) Halothane (H) group; they received MMA and 1% halothane. (4) Isoflurane (I) group; they received MMA and 1.5% isoflurane. (5) Sevoflurane (S) group; they received MMA and 2.5% sevoflurane. MMA 1000 micrograms/ml was administered 7 min after the start of perfusion except in the C group. At the end of the experimental period, the hearts were freeze-clamped and then myocardial high energy phosphates, lactate and glycogen were measured. Cardiac output in all groups but C group decreased significantly. PO2 of the perfusion blood in the M, H, I and S groups was significantly lower than that in the C group. Myocardial ATP in the M, H, I and S groups was significantly lower than that in the C group. ADP and AMP in the M, H, I and S groups were higher than those in the C group. There were no significant differences in lactate and glycogen levels between the 5 groups. MMA 1000 micrograms/ml is much higher than the blood level (0.05-31.89 micrograms/ml) which was reported in clinical patients who had femoral prosthesis. Therefore, the direct contribution of MMA itself to cardiac depression may be less than the other factors such as embolism in clinical situations. Volatile anesthetics did not influence the deleterious effects of MMA on cardiac function and metabolism.
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PMID:Cardiac effects of methylmethacrylate in the rat heart-lung preparation with or without volatile anesthetics. 886 19


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