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)

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.
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PMID:Pulmonary function changes induced by experimental dichlorvos toxicosis in calves. 373 27

The effects of tubocurarine 0.06 mg kg-1, alcuronium 0.03 mg kg-1, pancuronium 0.01 mg kg-1, and fentanyl 1 or 2 micrograms kg-1 on the muscle fasciculations associated with suxamethonium were studied in 171 children undergoing otolaryngological surgery. The mean fasciculation index in all pretreatment groups was significantly smaller than in the control group. The most effective pretreatment was fentanyl 2 micrograms kg-1 followed, in order, by alcuronium, fentanyl 1 microgram kg-1, tubocurarine and pancuronium. The rate of the onset of the fasciculations after the injection of suxamethonium ranged from 8 s after pancuronium to 20 s after tubocurarine. There was evidence of respiratory depression in the children receiving fentanyl 2 micrograms kg-1 if the duration of anaesthesia was less than 30 min.
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PMID:Effect of competitive myoneural blockade and fentanyl on muscle fasciculation caused by suxamethonium in children. 688 13

Cell adhesion molecules play important roles in axon guidance and synapse formation. Recent studies suggest that the expression of some of these molecules can be regulated either by electrical activity or by specific neurotransmitters. The expression of neural cell adhesion molecule (NCAM)-like molecules in Aplysia, designated apCAM, is downregulated from the surface of sensory neurons by 5-HT, a transmitter known to evoke long-term changes in the structure and function of these neurons. We tested whether the distribution of apCAM on the surface of other neurons can be regulated by treatments with other neurotransmitters known to evoke long-term functional and structural changes in Aplysia neurons, and we examined the consequences of treatments with the neurotransmitters on the pattern of growth cone-neurite interactions. We report that applications of the neuropeptide Phe-Met-Arg-Phe-amide (FMRFamide) that evoke long-term synaptic depression also reduce apCAM expression on the surface of motor cell L7 via a mechanism that appears to be similar to the mechanism mediating the 5-HT-induced change in the sensory cells. Specific treatments that affect apCAM distribution on the surface of their respective cells, 5-HT on sensory cells or FMRFamide on motor cell L7, mimic treatment with monoclonal antibodies against apCAM by evoking a significant reduction in the fasciculation of growth cones with other neurites extending from homologous cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decrease in growth cone-neurite fasciculation by sensory or motor cells in vitro accompanies downregulation of Aplysia cell adhesion molecules by neurotransmitters. 790 62

The extent to which cardiorespiratory infirmity and other sublethal effects of saxitoxin (STX) and tetrodotoxin (TTX) can be reversed by 4-aminopyridine (4-AP) was investigated in guinea pigs chronically instrumented for the concurrent electrophysiological recordings of electrocorticogram (ECoG), diaphragmatic electromyogram (DEMG), Lead II electrocardiogram, and neck skeletal muscle electromyogram. Animals were intoxicated with either STX or TTX (2 and 3 microg/kg, im) to produce a state of progressive cardiorespiratory depression (depicted by decreasing DEMG amplitude, bradypnea, and bradycardia). At the point where cardiorespiratory performance was most seriously compromised (approximately 30 min posttoxin), 4-AP (1 or 2 mg/kg, im) was administered. The therapeutic effect of 4-AP was striking in that, within minutes, the toxin-induced diaphragmatic blockade, bradypnea, bradycardia, and depressed cortical activity were all restored to a level either comparable to, or surpassing, that of control. The optimal 4-AP dose level was determined to be 2 mg/kg (im) based on analyses of cardiorespiratory activity profiles throughout the course of intoxication and 4-AP treatment. At the dose levels (either 1 or 2 mg/kg) used to restore ventilatory function and cardiovascular performance, 4-AP produced no sign of seizures and convulsions. Although less serious secondary effects such as cortical excitant/arousal effect (indicated by ECoG power spectral analysis) and transient periods of skeletal muscle fasciculation were observed, these events were of minor concern particularly in view of the remarkable therapeutic effects of 4-AP.
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PMID:4-Aminopyridine reverses saxitoxin (STX)- and tetrodotoxin (TTX)-induced cardiorespiratory depression in chronically instrumented guinea pigs. 926 7

Aldicarb (2-methyl-2(methylthio) propanal o-[(methylamino)-carbonyl] oxime) is a pesticide manufactured since 1965. This carbamate ester is sold under the tradename, Temik, and is used as insecticide and nematicide. The Environmental Protection Agency has classified aldicarb in the highest toxicity category and has defined a strict control for its delivery and use. In Brazil and the Caribbean island, aldicarb is illegally used as a household rodenticide with a widespread risk of poisoning. Our study presents the first review of aldicarb poisoning circumstances associated with clinical and analytical findings. Moreover, the oxime treatment is discussed. Eighteen patients with cholinergic symptoms admitted to the Emergency Unit and two deceased with a history of aldicarb poisoning were included in the study. As agricultural workers, only two of them could legally use Temik. Seventy percent of the patients was managed by the Emergency Mobil Unit. Serum cholinesterase activity was always lower than 30% of the normal range and aldicarb was identified by UV spectra and retention time after liquid chromatography separation. The most common muscarinic effect was diarrhea, the main nicotinic sign fasciculation and almost half of the poisoned patients had central nervous system (CNS) depression (Glasgow Coma Score lower than 8). Four patients had serious conduction abnormalities and two of them died. These results suggest that aldicarb intoxication is always severe. Oxime treatment did not produce side effects and should be recommended whenever the pesticide involved is unknown. Effective measures should be implemented to stamp out the illicit use of aldicarb.
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PMID:Aldicarb poisoning. 1129 36

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

NCAM, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation, axon outgrowth and fasciculation, and synaptic plasticity. To dissociate the functional roles of NCAM in the adult brain from developmental abnormalities, we generated a mutant in which the NCAM gene is inactivated by cre-recombinase under the control of the calcium-calmodulin-dependent kinase II promoter, resulting in reduction of NCAM expression predominantly in the hippocampus. This mutant (NCAMff+) did not show the overt morphological and behavioral abnormalities previously observed in constitutive NCAM-deficient (NCAM-/-) mice. However, similar to the NCAM-/- mouse, a reduction in long-term potentiation (LTP) in the CA1 region of the hippocampus was revealed. Long-term depression was also abolished in NCAMff+ mice. The deficit in LTP could be rescued by elevation of extracellular Ca2+ concentrations from 1.5 or 2.0 to 2.5 mm, suggesting an involvement of NCAM in regulation of Ca2+-dependent signaling during LTP. Contrary to the NCAM-/- mouse, LTP in the CA3 region was normal, consistent with normal mossy fiber lamination in NCAMff+ as opposed to abnormal lamination in NCAM-/- mice. NCAMff+ mutants did not show general deficits in short- and long-term memory in global landmark navigation in the water maze but were delayed in the acquisition of precise spatial orientation, a deficit that could be overcome by training. Thus, mice conditionally deficient in hippocampal NCAM expression in the adult share certain abnormalities characteristic of NCAM-/- mice, highlighting the role of NCAM in the regulation of synaptic plasticity in the CA1 region.
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PMID:Conditional ablation of the neural cell adhesion molecule reduces precision of spatial learning, long-term potentiation, and depression in the CA1 subfield of mouse hippocampus. 1497 28

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
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PMID:Poisoning due to chlorophenoxy herbicides. 1557 61

Chemical restraint is an important tool for the management and medical care of both captive and free-ranging rhinoceroses. Current anesthetic protocols for the white rhinoceros (Ceratotherium simum) are reported to cause varying degrees of hypertension, tachycardia, muscular stiffness and fasciculation, acidosis, and, most importantly, respiratory depression with resulting hypoventilation, hypoxia, and hypercapnea. To assist in the assessment and development of new and improved anesthetic techniques for the white rhinoceros, the following cardiopulmonary reference parameters for standing, unrestrained white rhinoceroses were generated (mean +/- standard error [minimum maximum]): heart rate = 39 +/- 0.8 beats/min (32-42), respiratory rate = 19 +/- 0.6 breaths/min (16-23), corrected indirect systolic blood pressure = 160 +/- 2.9 mm Hg (146-183), corrected indirect diastolic blood pressure = 104 +/- 2.3 mm Hg (88-117), corrected indirect mean blood pressure = 124 +/- 2.2 mm Hg (108-135), end tidal CO2 = 45.1 +/- 0.7 mm Hg (41.7-48.0), rectal temperature = 36.8 +/- 0.1 degrees C (36.6-37.2), arterial blood pH = 7.391 +/- 0.007 (7.346-7.431), arterial partial pressure of oxygen = 98.2 +/- 1.4 mm Hg (90.2-108.6), arterial partial pressure of CO2 = 49.0 +/- 0.9 mm Hg (44.4-53.7), base excess = 3.5 +/- 0.4 mmol/L (1.9-5.9), bicarbonate = 29.3 +/- 0.4 mmol/L (27.3-32.2), and arterial hemoglobin oxygen saturation (SaO2) = 97.2 +/- 0.1% (96.6-98.0).
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PMID:Reference cardiopulmonary physiologic parameters for standing, unrestrained white rhinoceroses (Ceratotherium simum). 1793 45

The objective of this study was to determine the level of anesthesia attained in Xenopus laevis frogs using a propofol bath administration. Thirty-three nonbreeding female Xenopus laevis frogs were used. At 175 mg/l, all frogs died after bath administration. An appropriate anesthetic dose was determined to be 88 mg/l for 15 min. After administration of this dose, the acetic acid test, withdrawal reflex, righting reflex, heart rate, and respiratory frequency were used to evaluate central nervous system depression. Pharmacokinetics of propofol were calculated after blood concentration determination by tandem liquid chromatography-mass spectrometry analyses. Short-duration anesthesia (less than 30 min) was obtained, and in many frogs, muscular fasciculation was seen during the acetic acid test. The area under the time-concentration curve (AUC0-t) was 24.07 microg.min/ml, and AUCinf was 24.71 microg.min/ml. The elimination half-life was 1.18 h. When administered as a single-bath immersion for 15 min, propofol does not appear to be a safe and effective anesthetic for Xenopus laevis frogs, due to a narrow dose-effect window, short duration, and shallow level of anesthesia obtained.
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PMID:Anesthetic properties of propofol in African clawed frogs (Xenopus laevis). 1894 68


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