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)

Mivacurium is a new short-acting competitive neuromuscular blocking agent. Infusion requirements for the maintenance of a stable 90-99% muscle twitch depression were determined in 28 children anaesthetized with nitrous oxide and 1% halothane (inspired) in oxygen or nitrous oxide in oxygen and opioid. Neuromuscular block was assessed by monitoring the force of contraction of the adductor of the thumb during train-of-four (TOF) stimulation at 0.1 Hz. Infusion rate and twitch depression were analysed from 15 to 75 min and from 75 to 135 min after the start of the infusion. In the first period of evaluation, the mean infusion requirement was 10.4 (SEM 0.92) micrograms kg-1 min-1 during the halothane anaesthesia and 13 (1.4) micrograms kg-1 min-1 during the opiod anaesthesia (P less than 0.05). This difference was present also during the second 60-min period. There was no significant correlation between infusion rates required to maintain greater than 90% depression of the first twitch (T1) of the TOF and plasma cholinesterase concentrations. Regardless of the anaesthetic regimen, children recovered rapidly after discontinuing the infusion. The recovery index (25-75% recovery of T1) for all patients was 5.4 (0.57) min with no significant differences between the groups.
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PMID:Continuous infusion of mivacurium in children. 253 33

In this paper the activity of blood cholinesterase and serum cholinesterase were reported in 32 depressions without physical disease. There were 20 males and 12 females. Prior to study none of the patients received antidepressants, lithium and antipsychotics or other therapies. The control group consisted of 43 normal healthy persons (male: 32, female: 11). The results showed that the mean activity unit of blood cholinesterase and serum cholinesterase were lower in major depression than in the control group. Particularly more lower in the activity of blood cholinesterase in patients with very severe depression and longer course of depression. The differences were statistically significant. Based on the review of literatures, some authors suggested that the low activity of blood cholinesterase would be consistent with the hypothesis, that depression is associated with reduced cholinesterase activity in the brain. The reason for the mechanism is not clear. Whether it is a biological marker of depression, this needs further investigation.
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PMID:[The preliminary investigation of cholinesterase in depression]. 262 May 92

The measurement of plasma and erythrocyte cholinesterase activities is used to monitor absorption of anti-cholinesterase organo-phosphorus compounds. A fall in an individual's enzyme activity signifies excessive exposure if it is clearly greater than the normal intra-individual variation found in unexposed subjects. The extent of normal variation in enzyme activity as measured is dependent on both the true intra-individual biological variation and the precision of the method used. This report defines normal variation in plasma and erythrocyte cholinesterase activity using the assay developed and used routinely in our laboratory. We have also defined the relation between the precision of the assay used by a laboratory and the sensitivity with which a significant depression in successive enzyme measurements can be detected. This allows occupational physicians, who use cholinesterase measurements to monitor organo-phosphate exposure, to establish percentage depressions from their method precision data that may possibly indicate organo-phosphate uptake between successive enzyme measurements. We have calculated that, with our analytical precision, percentage drops between two successive measurements that are greater than 15 and 7.5 per cent for the plasma and erythrocyte enzymes respectively suggest significant organo-phosphorus absorption in pesticide workers.
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PMID:Intra-individual variation in plasma and erythrocyte cholinesterase activities and the monitoring of uptake of organo-phosphate pesticides. 262 38

The authors investigated in human and in experimental organophosphate intoxication the features of the toxic ECG repolarisation disturbance, the QT lengthening and its connection with cholinesterase depression. It was concluded that this pathological electrophysiological change in human intoxication does not show close correlation with the decrease of enzyme activity and cannot be influenced by atropine. The ECG alteration can be reproduced in animal experiments, it precedes the toxicologically relevant cholinesterase depression, it is pesticide dose dependent, but it cannot be induced by cholinergic or adrenergic drugs. On the basis of all this it is supposed that in organophosphate intoxication the QT lengthening reflects a direct myocardial pesticide effect and, is independent of cholinergic mediation.
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PMID:[ECG repolarization disorder (QT lengthening) in organophosphate poisoning]. 264 83

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Five incidences of bird mortality in Georgia and West Virginia (USA) involving migratory waterfowl, cranes, raptors, corvids and songbirds were investigated during the first 6 mo of 1988. Gross and histopathologic examinations revealed no evidence of infectious or other diseases. However, severe depression of cholinesterase activity was evident in brains of birds found dead, suggesting gross exposure to an organophosphorus (OP) or carbamate pesticide. All of the gastrointestinal tract contents chemically analyzed contained famphur, an OP insecticide used as a pour-on treatment against lice and grubs on livestock, ranging from 5 to 1,480 ppm (wet weight). Grain scattered at two of the mortality sites contained 4,240 and 8,500 ppm famphur. Gastrointestinal tracts of most of the dead birds contained mainly corn and some wheat. This is the first report to document the use of famphur as an intentional means of killing wildlife thought to be depredating crops.
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PMID:Case histories of wild birds killed intentionally with famphur in Georgia and West Virginia. 271 98

Eight-month-old Jersey bull calves given ivermectin intravenously or subcutaneously showed signs of depression, ataxia, difficulty in breathing, tachycardia, salivation, diarrhoea, miosis, and an increase in pseudocholinesterase activity. The clinical signs were severe in calves given the drug intravenously. The findings suggest that the cholinergic nervous system may be involved in some of the adverse effects of ivermectin observed in calves.
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PMID:Clinical signs and biochemical changes in calves caused by injection of ivermectin. 271 47

The ability of physostigmine (PHY) and pyridostigmine (PYR) to protect against the segmental synaptic depression caused by sarin was examined in isolated spinal cords from neonatal rats. The monosynaptic reflex was unaffected at concentrations up to 0.1 microM PHY or 0.3 microM PYR but raising the concentrations of either drug produced a concentration-dependent depression of the monosynaptic reflex which could be completely antagonized by atropine. The monosynaptic reflex was depressed by 50% at 0.45 microM PHY and 2 microM PYR with maximal depression occurring at 1 microM PHY (to about 10% of control) and 10 microM PYR (to about 35% of control). Pretreating the cords with 0.1 microM PHY and PYR for 30 min failed to protect against the depressant effects of sarin even though they inhibited total cholinesterase (ChE) by 27 and 21%, respectively. Both PHY and PYR depressed total ChE activity of the spinal cord in a concentration-dependent manner with 50% inhibition of ChE occurring at 0.8 microM. These results suggest that the carbamates affect segmental transmission by activation of a muscarinic receptor, that protective carbamylation of ChE is ineffective against organophosphorus-induced segmental depression, and that inhibition of ChE is unrelated to both carbamate- and organophosphorus-induced depression of the monosynaptic reflex.
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PMID:Interaction of reversible and irreversible cholinesterase inhibitors on the monosynaptic reflex in neonatal rats. 272 98

We have studied the action of doxapram on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation. Doxapram augmented neuromuscular transmission in a dose-related manner when a threshold concentration of 5 x 10(-5) mol litre-1 had been exceeded. The activity of the acetylcholinesterase in rat diaphragm has been examined also in the presence of doxapram. No inhibitory effect was seen in the concentration range which augmented neuromuscular transmission, thus excluding cholinesterase inhibition as the underlying mechanism. In contrast, in the presence of partial neuromuscular block, a dose-related depression of neuromuscular transmission with doxapram was revealed. This was greatest when the neuromuscular blocking agents possessed significant presynaptic activity (beta-bungarotoxin and tubocurarine). In this situation any facilitatory action of doxapram was severely reduced or abolished. In contrast, the facilitatory effects of doxapram were apparent in the presence of partial block produced by agents with less or no presynaptic activity (pancuronium and alpha-bungarotoxin). This study suggests that doxapram has a presynaptic facilitatory action at the neuromuscular junction. In the presence of partial neuromuscular block, an inhibitory action is revealed which may be post-junctional. The concentrations of doxapram at which these effects appear are approximately five times greater than those reached in plasma after a standard clinical dose.
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PMID:Doxapram and the neuromuscular junction. 231 31

Exogenously applied muscarinic agonists--for example, acetylcholine (ACh) and acetyl-beta-methacholine (MCh)--modify frequency receptive fields in auditory cortex of unanesthetized animals in a frequency-specific rather than global manner. The present study sought to relate these findings to endogenous actions of ACh by using the anticholinesterase agents eserine sulphate and soman (0-1,2,2-trimethylpropylmethylphosphonofluoridate) to facilitate the effects of endogenous ACh. Frequency receptive fields (FRF) were determined by presenting sequences of different isointensity tones before, during, and after application of ACh, MCh, eserine, or soman; also the cholinesterase blockers were applied between applications of ACh or MCh. The major effects produced by the inhibitors were similar to those of the agonists. Predominant effects were frequency-specific changes in FRF. Further, eserine and soman, similar to ACh and MCh, produced shifts in the best frequency (BF) of FRF due mainly to coordinated depression of responses to the BF and increased responses to adjacent, non-BF. The results indicate that exogenous and endogenous ACh, acting via muscarinic receptors, can significantly influence the physiological functioning of cortical neurons and consequently their processing of sensory information.
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PMID:Cholinergic modulation of frequency receptive fields in auditory cortex: II. Frequency-specific effects of anticholinesterases provide evidence for a modulatory action of endogenous ACh. 277 38


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