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

Improved understanding of the structure/activity relationship of inhaled anaesthetics has resulted in the synthesis of fluorinated compounds which are more potent and less toxic than their unfluorinated antecedents. The toxic effects of inhaled anaesthetics on the liver and kidney are complex but, in general, are related to the extent to which individual inhaled agents are metabolised. Halothane hepatotoxicity is a rare, idiosyncratic reaction which typically occurs in obese women having more than one exposure to the drug within a short time interval. All currently available volatile anaesthetic drugs have depressant effects on the cardiovascular and respiratory systems; arrhythmias are more likely with halothane than with the fluorinated ethers. Cerebral blood flow tends to increase during inhalation anaesthesia, especially with halothane and in the presence of hypercarbia; isoflurane may be given sparingly during neurosurgical procedures whilst monitoring its end-tidal concentration. Although the volatile agents tend to cause uterine relaxation they may be given safely in low concentration to avoid awareness during Caesarean section. In general, young children require rather higher concentrations of volatile agents than adults and seem to be less susceptible to organ toxicity. Two relatively new volatile agents, sevoflurane and desflurane, offer some advantages over isoflurane but neither is an "ideal drug'. Sevoflurane interacts with soda-lime to produce a series of degradation products, the most important of which is compound A. Production is greatest during low-flow, closed circuit anaesthesia using high inspired concentrations of the drug. Compound A has nephrotoxic potential in rats but the clinical significance of the interaction between sevoflurane and soda-lime is unclear. Nitrous oxide when given for prolonged periods may cause irreversible bone marrow depression.
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PMID:Comparative tolerability profiles of the inhaled anaesthetics. 909 54

1969 Sevofluran was synthesized and in December 1995 licensed for clinical use in Germany. The low blood/gas partition coefficient is responsible for the fast uptake and elimination of sevoflurane. Sevoflurane does not irritate the airway. In human medicine no side effect of liver- and kidney function have been seen after sevofluran anaesthesia. There is low cardiovascular and respiratory depression caused by sevoflurane. In this study the use of sevoflurane in dogs should be tested and compared with isoflurane and halothane anaesthesia. All dogs were premedicated with /-methadon and diazepam. No significant depression of the cardiovascular system was seen. Neither kidney-nor hepatotoxic side effects could be found after sevoflurane, isoflurane and halothane anaesthesia. After sevoflurane anaesthesia the dogs woke up quietly and without any excitation and were able to stand on average ten minutes earlier after sevoflurane anaesthesia than after isoflurane and 85 minutes earlier than after halothane anaesthesia.
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PMID:[Sevoflurane (SEVOrane) as an inhalation anesthetic in dogs in comparison with halothane and isoflurane]. 985 16

In common with other halogenated volatile anaesthetics, sevoflurane causes a dose-related cardiovascular depression and therefore the affection of blood flow of different organ systems is suggested. So far known, sevoflurane is not different compared to isoflurane in affecting liver and splanchnic blood flow. Concluded from former published studies there was no case of hepatic toxicity of sevoflurane been published so that this substance can be used in patients with reduced hepatic function. The primary organic metabolite of sevoflurane is hexafluorisopropanol (HFIP), which is readily and rapidly conjugated with glucuronic acid. No reactive intermediates are formed and HFIP appears to be an unlikely compound to form liver protein adducts. For this reasons sevoflurane "hepatitis" is not expected. Like most other inhalation agents sevoflurane increase the neuromuscular blockade after treatment with muscle relaxants in anaesthesia. The MAC values of Sevoflurane where reduced after the application of nitrous oxide, benzodiazepines and opiates. From human studies we know that chronic drug therapy with isoniazid induces the metabolism of sevoflurane, enflurane and isoflurane, markedly increasing peak plasma fluoride concentrations. However, barbiturates as well as phenytoin do not influence the metabolism of sevoflurane because these agents do not induce the major hepatic defluorinating enzyme cytochrome P450 2E1. Obesity, untreated diabetes mellitus and alcohol abuse increase the hepatic content and activity of cytochrome P450 2E1 and therefore enhanced anaesthetic defluorination is to be suspected. Until now, there are no studies about sevoflurane anaesthesia in patients after liver transplantation but the extremely low hepatotoxic potential as compared to isoflurane provides no argument to avoid this substance for anesthesia in liver transplanted patients.
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PMID:[Perfusion and metabolism of liver and splanchnic nerve area under sevoflurane anesthesia]. 989 76

The cellular and synaptic mechanisms by which general anesthetics affect cell-cell communications in the nervous system remain poorly defined. In this study, we sought to determine how clinically relevant concentrations of sevoflurane affected inhibitory synaptic transmission between identified Lymnaea neurons in vitro. Inhibitory synapses were reconstructed in cell culture, between the somata of two functionally well-characterized neurons, right pedal dorsal 1 (RPeD1, the giant dopaminergic neuron) and visceral dorsal 4 (VD4). Clinically relevant concentrations of sevoflurane (1-4%) were tested for their effects on synaptic transmission and the intrinsic membrane properties of soma-soma paired cells. RPeD1- induced inhibitory postsynaptic potentials (IPSPs) in VD4 were completely and reversibly blocked by sevoflurane (4%). Sevoflurane also suppressed action potentials in both RPeD1 and VD4 cells. To determine whether the anesthetic-induced synaptic depression involved postsynaptic transmitter receptors, dopamine was pressure applied to VD4, either in the presence or absence of sevoflurane. Dopamine (10(-]5) M) activated a voltage-insensitive K(+) current in VD4. The same K(+) current was also altered by sevoflurane; however, the effects of two compounds were nonadditive. Because transmitter release from RPeD1 requires Ca(2+) influx through voltage-gated Ca(2+) channels, we next tested whether the anesthetic-induced synaptic depression involved these channels. Individually isolated RPeD1 somata were whole cell voltage clamped, and Ca(2+) currents were analyzed in control and various anesthetic conditions. Clinically relevant concentrations of sevoflurane did not significantly affect voltage-activated Ca(2+) channels in RPeD1. Taken together, this study provides the first direct evidence that sevoflurane-induced synaptic depression involves both pre- and postsynaptic ion channels.
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PMID:Sevoflurane induced suppression of inhibitory synaptic transmission between soma-soma paired Lymnaea neurons. 1056 48

Sevoflurane and Desflurane are relatively new halogenated agents which make induction and control of depth of anaesthesia easier, recovery rapid and of good quality and they have less side-effects and toxicity. In children sevoflurane could replace halothane because it provides smooth and rapid induction with less cardiovascular depression and arrhythmias. Desflurane is not used because of its pungent odour. In adults sevoflurane could be preferred to desflurane because it allows rapid induction and laryngeal mask insertion or tracheal intubation without myorelaxants, a similar time of recovery, no clinical evidence for renal and hepatic toxicity, no more costs for anaesthesia for a lower MAC.
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PMID:New halogenated agents: should I change my practice? 1096 99

The volatile anaesthetic agents are known to influence uterine muscle tone. All of the agents studied to date have been found to produce uterine relaxation. This property has been used to produce therapeutic uterine relaxation for difficult obstetric deliveries and the Ex Utero Intrapartum Treatment (EXIT) procedure. This study describes the effects of sevoflurane on isolated human myometrium at concentrations of 0.1, 0.25, 0.5, 0.75, 1.0, 1.5, 2.5 and 3.5 MAC. Sevoflurane produces dose-dependent depression of uterine muscle contractility with an ED50 of 0.94 MAC. Frequency of contraction was increased at concentrations of 2.5 MAC and greater. At concentrations of 3.5 MAC and above, uterine activity was virtually abolished.
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PMID:The effects of sevoflurane on isolated gravid human myometrium. 1241 58

Sevoflurane is the latest halogenated ether introduced in clinical anaesthesia, and its effects at the spinal level are not fully characterised. The rat hemisected spinal cord preparation was used to test the effects of sevoflurane on spinal nociceptive and non-nociceptive synaptic transmission as well as on excitations produced by application of glutamate-receptor agonists. Sevoflurane was dissolved in artificial cerebrospinal fluid (ACSF) with a specific vaporiser, and its final concentration was assessed with gas chromatography. Sevoflurane reduced the mono-synaptic reflex (EC(50) approximately 219 microM) and the slow components of the dorsal root-ventral root potentials (EC(50) approximately 72 microM) elicited by single dorsal root stimulation as well as the cumulative depolarisation (CD) elicited by repetitive stimulation (EC(50) approximately 98 microM). AMPA- and NMDA-induced depolarisations were also reduced by sevoflurane (respective EC(50)s were 206 and 127 microM). Inhibition of NMDA-induced depolarisation was TTX resistant. However, complete blockade of NMDA receptors with d-AP5 did not prevent further reduction of the CD by sevoflurane. All the effects reported were concentration-dependent and reversible. We conclude that sevoflurane applied at clinically relevant concentrations induces a strong depression of nociceptive and non-nociceptive spinal systems, which may be partly mediated by interfering with excitatory amino acid transmission.
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PMID:Characterisation of sevoflurane effects on spinal somato-motor nociceptive and non-nociceptive transmission in neonatal rat spinal cord: an electrophysiological study in vitro. 1268 79

Electroconvulsive therapy is an effective treatment for severe and medication-resistant depression. There have been no reports describing how a volatile anaesthetic affects haemodynamic responses, seizure duration, and recovery characteristics during electroconvulsive therapy. We carried out a repeated-measure crossover study to compare the effects on haemodynamic responses, seizure duration, and recovery characteristics of the following types of anaesthesia in electroconvulsive therapy: propofol alone, sevoflurane alone, and propofol combined with sevoflurane. We recruited 50 patients requiring electroconvulsive therapy for depression. For anaesthesia induction, 1.5 mg/kg propofol (condition P), 5% sevoflurane in oxygen following a vital capacity rapid inhalation induction (condition S), or 1.5 mg/kg propofol followed by 5% sevoflurane in oxygen (condition PS) was administered. Succinylcholine 1.5 mg/kg was then given. Electrical stimulation was administered after fasciculation. Measurements were obtained before anaesthesia induction (baseline), prior to succinylcholine administration, prior to electroconvulsive therapy, and at the peak after electroconvulsive therapy. After electroconvulsive therapy, peak heart rate and peak mean arterial pressure were highest in condition S. Whereas recovery time was longest in condition PS, motor seizure duration was significantly shorter than in either condition P or S. Electroencephalographic seizure duration was significantly shorter in condition PS than in condition P and significantly shorter in condition S than in condition P. Sevoflurane anaesthesia alone is most disadvantageous in terms of haemodynamics. Propofol-sevoflurane anaesthesia is advantageous in terms of haemodynamics, but disadvantageous in terms of seizure duration and recovery time. Propofol alone is most advantageous in terms of seizure duration.
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PMID:Propofol alone, sevoflurane alone, and combined propofol-sevoflurane anaesthesia in electroconvulsive therapy. 1297 63

The effects of 2.5% and 5% of sevoflurane anesthesia on hemodynamics and myocardial metabolism were studied in pentobarbital-pancuronium anesthetized dogs. The interaction between nicardipine and 2.5% sevoflurane was also examined. Sevoflurane produced dose-dependent ( P << 0.05 to P << 0.01) decreases in systolic arterial pressure (SAP), heart rate (HR), cardiac index (CI), left ventricular minute work index (LVMWI), maximum rate of rise of left ventricular pressure (LV dP/dt), the time constant of fall in isovolumic left ventricular pressure (T) and systemic vascular resistance (SVR), whereas stroke volume index (SVI) and left ventricular end-diastolic pressure (LVEDP) remained unchanged. Central venous pressure (CVP) was significantly ( P << 0.05) increased at 5%. Myocardial oxygen consumption (MV(O)(2)), and myocardial lactate extraction ratio (ML ext) were decreased in a dose-dependent manner ( P << 0.05). Myocardial oxygen extraction ratio (M(O)(2) ext) was significantly ( P << 0.01) decreased at 5%. The ratio of the left ventricular minute work index to myocardial oxygen consumption (LVMWI/MV(O)(2)), i.e., left ventricular efficiency was significantly decreased only at 5% ( P << 0.05). Coronary sinus blood flow (CSBF) was significantly ( P << 0.05) decreased only at 2.5% sevoflurane and coronary vascular resistance (CVR) was significantly ( P << 0.01) decreased only at 5% sevoflurane. The ratio of CSBF to CO (CSBF/CO) showed a tendency to increase as sevoflurane concentrations were increased. Nicardipine (0.01 mg.kg(-1)) administered intravenously under 2.5% sevoflurane caused significant ( P << 0.05 to P << 0.01) decreases in SAP, HR, LV dP/dt, SVR, and CVR, and increases in CVP, SVI, CI, and CSBF ( P << 0.05 to P << 0.01). CSBF/CO remained unchanged. MV(O)(2), M(O)(2) ext, and ML ext were significantly ( P << 0.05 to P << 0.01) decreased. LVMWI/MV(O)(2) showed a tendency to increase. It is concluded that sevoflurane causes a rapidly and easily controlled cardiovascular depression and may not have unfavorable effects on coronary circulation and myocardial metabolism. Nicardipine exerts a synergistic myocardial depressant effect on sevoflurane, in terms of both cardiovascular dynamics and myocardial metabolism.
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PMID:Effects of sevoflurane on cardiovascular dynamics, coronary circulation and myocardial metabolism in dogs. 1523 85

Sevoflurane was compared to isoflurane anesthesia alone and in combination with atracurium or vecuronium in 84 rats using the sciatic nerve-anterior tibialis muscle preparation. Both bolus injection and infusion rate techniques were used to evaluate these drug interactions. The ED(50) (dose which produced a 50% depression of twitch tension) of atracurium was 311 +/- 31 and 360 +/- 32 microg.kg(-1) during 1.25 MAC sevoflurane and isoflurane anesthesia respectively. The ED(50) of vecuronium was 190 +/- 27 and 149 +/- 14 microg.kg(-1) during 1.25 MAC sevoflurane and isoflurane anesthesia respectively. The mean infusion rates of atracurium and vecuronium required to maintain a 50% depression of twitch tension were 5.04 +/- 0.7 and 2.02 +/- 0.3 mg.kg(-1).hr(-1). These infusion rates were 5.04 +/- 0.7 and 2.02 +/- 0.3 mg.kg(-1).hr(-1) during 1.25 MAC sevoflurane and 3.73 +/- 0.3 and 1.81 +/- 0.4 mg.kg(-1).hr(-1) during 1.25 MAC isoflurane anesthesia respectively. With both atracurium and vecuronium, the infusion rate required to maintain a 50% depression twitch of tension was inversely related to the concentrations of isoflurane and sevoflurane. The authors conclude that sevoflurane is similar in potency to that of isoflurane in augmenting a vecuronium or atracurium induced neuromuscular blockade in a dose-dependent manner.
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PMID:The neuromuscular effects of sevoflurane and isoflurane alone and in combination with vecuronium or atracurium in the rat. 1527 76


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