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)

Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered by infusion to 10 cats that were anesthetized with isoflurane and oxygen to allow transplantation of a myocutaneous flap. Five of the cats were given cyclosporine (20 mg/kg of body weight, PO q 12 h in divided doses) for 2 days prior to anesthesia, and prednisolone (0.25 mg/kg, PO) on the morning of surgery. The other 5 cats were not given either drug. Neuromuscular blockade was assessed, using the train-of-four stimulation, and throughout surgery, the infusion rate was adjusted to maintain the first-twitch response (T1) at 90 to 95% depression from baseline. At completion of surgery, atracurium was discontinued, and the infusion rate and the time for recovery (the time for the train-of-four ratio to increase from 50 to 75%) were recorded. Once the train-of-four ratio had been stable for 10 minutes, edrophonium (0.5 mg/kg), a cholinesterase inhibitor, was administered IV, and neuromuscular blockade was monitored for another 10 minutes. Mean (+/- SD) duration of the atracurium infusion was 302.1 +/- 70.5 minutes for the control group and was 323.9 +/- 61.7 minutes for the cats given cyclosporine and prednisolone. In the cats of the control group, the infusion rate required to induce 90 to 95% T1 depression from baseline was 3.7 +/- 0.7 micrograms/kg/min. This rate was not significantly different from that of 2.8 +/- 1.2 micrograms/kg/min in cats given cyclosporine and prednisolone. Significant difference in recovery time was not evident between the control group and the treated group (6.4 +/- 4.5 minutes vs 6.2 +/- 2.5 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atracurium administration, as an infusion, to induce neuromuscular blockade in clinically normal and temporarily immune-suppressed cats. 225 41

The biochemical and morphological effects of postnatal acetylcholinesterase (AChE) inhibition were examined in rat pups dosed with paration, at time points critical to hippocampal neurogenesis and synaptogenesis (i.e., day 5-20). In treated pups, sacrificed on day 21, hippocampal histopathology, as assessed by light and electron microscopy, consisted of cellular disruption and necrosis in the dentate gyrus (DG), and CA4 regions. Synaptic disruption in the DG molecular layer was suggested by histochemical preparation using both the Timm's and AChE stains. In parathion-treated pups, sampled at day 12, hippocampal AChE was depressed 73% and [3H] quinuclidiny benzilate (QNB) binding was depressed by 36%. The above results indicate that morphological and biochemical consequences are associated with persistent AChE depression in neonatal rats.
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PMID:The neurotoxicity of parathion-induced acetylcholinesterase inhibition in neonatal rats. 228 52

An illness characterized by weakness, dizziness, and gastrointestinal symtoms was identified among a crew of 30 migrant field-workers employed by a grape grower in Madera County, California, during August 1987. The onset of symptoms occurred between August 24 and August 30 and a median of 9 days from the date of first employment. The first crew member sought medical treatment on August 26, and 10 crew members were admitted to hospital between August 27 and August 30. For most workers, gastrointestinal and constitutional symptoms resolved shortly after admission, but 4 patients had episodes of severe sinus bradycardia persisting for several days. On the day of admission, transient atrioventricular dissociation developed in 2 persons. Interviews with 16 crew members not admitted to the hospital identified only 1 additional worker ill with gastrointestinal symptoms, but all 16 had moderate to severe inhibition of both plasma and red blood cell cholinesterase. Four other workers who were tested but not interviewed also had cholinesterase depression. The crew had had exposure since August 19 to the organophosphate insecticide phosalone, which was last applied to the vineyard on July 21, or 29 days earlier. Although this is the first report unequivocally linking phosalone to field-worker poisoning, the delayed onset and nonspecific nature of the symptoms associated with subacute poisoning may have hindered the recognition of previous similar episodes.
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PMID:Subacute poisoning with phosalone, an organophosphate insecticide. 229 66

Rats injected intravenously with monoclonal antibodies reactive with brain acetylcholinesterase (AChE) developed a prolonged depression of plasma AChE without changes in butyrylcholinesterase, lactic acid dehydrogenase, or hematocrit. One antibody, ZR1, accumulated in the brain and spinal cord. Within 3 days of injection, ZR1 bound to most of the AChE in cerebral cortex and certain other regions of the CNS. Examination of the molecular forms of cortical 10S AChE, whereas 4S AChE remained free. In vitro, however, ZR1 bound equally to solubilized 4S and 10S forms. These data provide direct evidence for the compartmentalization of different AChE forms in the CNS, 10S being mainly extracellular and 4S apparently intracellular. Development of a striking and persistent bilateral ptosis within hours of injection suggests that AChE in the autonomic nervous system is also accessible to antibodies and, furthermore, is the site of an immunopathological lesion. This novel model of cholinergic autoimmunity may have relevance for human neurological disorders of unknown etiology.
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PMID:Selective complexing of acetylcholinesterase in brain by intravenously administered monoclonal antibody. 229 14

Brain cholinesterase (ChE) activities of songbirds collected in pecan groves 6 to 7 hr after separate applications of the organophosphorus pesticides, phosalone and disulfoton, were compared to mean ChE activities of controls (normals) as a measure of insecticide exposure. In general, reduction of brain ChE activity greater than or equal to 2 standard deviations below the control mean indicates exposure to an anticholinesterase compound. Phosalone had little effect on brain ChE activity of birds from treated groves; only slight to moderate (21 to 38%) ChE inhibition was detected in blue jays (Cyanocitta cristata) and red-bellied woodpeckers (Melanerpes carolinus). However, 11 of 15 blue jays from disulfoton-treated groves had moderate to severe ChE depression, ranging from 32 to 72%. Inhibition greater than or equal to 50% of normal may be diagnostic for cause of death. Direct mortality was not observed, but studies have shown that bird carcasses disappear rapidly from agricultural areas, many within 24 hr. We recommend additional field studies of the effects of disulfoton to wildlife, since large wheat-growing areas in the western United States are being considered for disulfoton treatment to control the Russian wheat aphid (Diuraphis noxia).
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PMID:Brain cholinesterase inhibition in songbirds from pecan groves sprayed with phosalone and disulfoton. 230 90

A reference range for erythrocyte acetyl cholinesterase (EAChE) in 46 mentally normal subjects aged 65 years or over has been established. Previous reports of a relationship between changes in (EAChE) levels and mental illness (dementia and depression) in the elderly suggested that this determination may be useful in screening elderly subjects for these illnesses or as an aid to diagnostic classification. A study of normal and mentally ill elderly subjects in the community in Liverpool does not confirm a relationship with either senile dementia or depression and many of the changes in EAChE levels noted previously can be accounted for either by variations in the haematocrit or by a hitherto unreported lowering of EAChE levels in normal women over 80 years of age.
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PMID:Erythrocyte acetyl cholinesterase in elderly patients with dementia and depression compared with normal controls. 233 4

Four test groups of small songbirds (Zebra Finch, Poephila guttata) were sprayed in a chamber with varying concentrations of fenitrothion. Exposure levels were assessed by monitoring air concentrations, deposits of the active ingredient (AI) on glass plates and droplets/cm2 on Kromekote cards. All indices of exposure were linearly correlated and the mean AI deposit on glass plates for the four groups tested with equivalent to 38, 51, 139 and 255 g/ha or 14%, 18%, 50% and 91% of the highest permissible emitted rate for broadscale forest spraying in Canada. Significant depression in body weights and brain acetylcholinesterase levels were noted only for the highest exposure group. Fenitrothion residues in blood were detectable only at the highest exposure level, and in liver at the two higher levels. Carcass and feather residues were much higher than those in blood and liver, and were detectable at all exposure levels but the residues did not increase linearly with exposure. For one of the spray groups, we were able to compute an equivalent acute oral dose based on matching acetylcholinesterase inhibition.
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PMID:An improved method to study the impact of pesticide sprays on small song birds. 234 1

Depression of platelet function with a single intraperitoneal injection of acetylsalicylic acid was found to produce significant increases in several thrombocytopoietic indicators despite no observed change in platelet counts. There was an increase in the number of megakaryocytic precursor cells (small acetylcholinesterase positive or "SAChE+" cells), platelet size, and 35S incorporation into platelets. The results are qualitatively comparable to data from previous experiments showing that treatment of mice with a thrombocytopoiesis-stimulating factor (TSF or thrombopoietin) and rabbit anti-mouse platelet serum will elevate thrombocytopoiesis. The results presented herein indicate that interruption of platelet function by aspirin results in the production of new platelets, presumably by the action of a feedback system controlling thrombocytopoiesis.
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PMID:Acetylsalicylic acid stimulates murine megakaryocyte precursor cells. 235 90

Three outbreaks of food poisoning involving watermelons or cucumbers and caused by the carbamate pesticide aldicarb occurred in California between 1985 and 1988. For each outbreak, and for an outbreak of aldicarb poisoning associated with English cucumbers previously reported in the literature, dosages of aldicarb sulfoxide that caused the illnesses were estimated. Estimated dosages ranged between 0.0023 [corrected] and 0.06 mg/kg body weight, and most were well below the 0.025 mg/kg Lowest Observed Effect Level (LOEL) for subclinical blood cholinesterase depression previously reported for humans. These findings are consistent with aldicarb sulfoxide (ASO) illnesses that have occurred in other states. Aldicarb appears to be more toxic than previously suspected. Scientific and regulatory implications are discussed.
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PMID:Aldicarb food poisonings in California, 1985-1988: toxicity estimates for humans. 238 19

The mechanisms responsible for slowing cardiac impulse conduction through the atrioventricular (AV) node are not well understood but include anatomical architecture, presence of cells with diverse electrophysiological characteristics, and modulation by autonomic nervous system. The present study was designed to determine the site of vagally induced slowing of conduction through the AV node. We attempted to correlate the electrophysiological response of AV nodal cells to postganglionic vagal stimulation applied in different regions of the node with the morphological findings and patterns of acetylcholinesterase-positive staining of nodal tissue. This multifaceted approach revealed that vagal stimulation produced localized hyperpolarization of the cells from the N region of the AV node, which correlated with the strong acetylcholinesterase positive staining of the central nodal area. In contrast, the density of the acetylcholinesterase staining decreased toward both the AN and His bundle regions, whereas vagal stimulation had a negligible effect on the cells from these regions. These results suggest that vagal-induced depression of AV nodal conduction is produced by release of acetylcholine predominantly around the midnodal region and the depressive action of acetylcholine is concentrated on the cells occupying the same region (i.e., the N cells). Thus, there appears to be a close juxtaposition of nerve elements and effector cells in the midnodal region of the AV node. This unique combination of available neuromediator and responding cells with hyperpolarization and depressed action potential determines the midnodal region as the focus of vagal effect on AV nodal conduction.
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PMID:Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity. 239 13


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