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)

The convulsant effects of cocaine and its C2-epimer, pseudococaine on EEG, respiration, heart rate and behavior were studied in the rhesus monkeys with electrodes implanted in the brain. Intravenous injections of cocaine (3.0 to 8.0 mg/kg) and pseudococaine (3.0 to 7.0 mg/kg) in the animals produced a similar pattern of clonic convulsions accompanied by marked increases in the heart and respiratory rates with mydriasis and excessive salivation. However, both isomers showed different effects on the EEG and animal's behavior following convulsions; e.g., the cocaine-induced convulsions were followed by low-voltage fast waves in the EEGs associated with behavioral hyperexcitation, while pseudococaine-induced convulsions were followed by high-voltage slow waves associated with behavioral depression and drowsiness with intermittent sleep. Pseudococaine was more potent than cocaine in producing convulsions in the same monkeys. The durations of convulsions produced by these drugs were dose-dependent.
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PMID:Comparison of the convulsant effects of cocaine and pseudococaine in the rhesus monkey. 41 26

Acute dapsone poisoning is rare and such cases are either accidental or suicidal. Though accidental DDS poisoning are reported in children, the same is fairly uncommon in adults. Only 2 such cases are reported in India literature. We here report 4 cases of fatal sucidial DDS poisoning in adults resulting death in 3 cases. The reported acute symptoms include nausea, vomiting, hyperexcitability followed by depression, Carpopedal spasm or convulsions. The most marked signs are dyspnoea and cyanosis. The symptoms are due to methaemoglobinaemia, and or sulphaemoglobinaemia. Normally dapsone induces red cell haemolysis and even with small therapeutic doses of 25-100 mg per day, and in toxic doses reduces the oxygen carrying capacity of blood and damages the red cells making them more vulnerable for haemolysis. The peculiarity of the presentation in this series are manifestation of severe haemorrhagic episode in one case and progressive jaundice in another besides cyanosis. None of the cases had carpopedal spasm or convulsion. Out of four cases three died inspite of intensive care, intravenous vitamin C, exchange transfusion (2 cases) and other supportive measures. Intravenous methylene blue could not be used in these cases due to non-availability.
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PMID:Acute fatal DDS poisoning. (Report of 4 cases). 48 Sep 16

In contrast to other benzodiazepine, Ro 5-3663 produces convulsions in mice. The CD50 of 7.0 mg/kg i.v. falls between that of picrotoxin and pentylenetetrazol. An electrophysiological study was made of the effects of this convulsant benzodiazepine on spinal reflexes and on ganglionic depolarization evoked by gamma-aminobutyric acid (GABA). In the unanesthetized spinal cat, Ro 5-3663 (15 mg/kg i.v.)depressed the dorsal root potentials and abolished the dorsal root reflexes evoked by muscle and cutaneous afferent inputs. The monosynaptic reflex was typically depressed, whereas polysynaptic potentials were enhanced. Diazepam reversed the depression of the dorsal root reflex and dorsal root potential produced by the convulsant benzodiazepine and reduced the enhancement of the polysynaptic potential. Presynaptic inhibition was attenuated by the convulsant, whereas strychnine-sensitive postsynaptic inhibition was slightly potentiated. Ro 5-3663 reduced the amplitude and duration of the GABA-evoked negative surface potential recorded from the superior cervical ganglion. The results indicate that the convulsant benzodiazepine acts in an opposite manner to the depressant benzodiazepines and support the hypothesis that these two types of compounds act through a modulation of GABAergic mechanisms.
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PMID:Reduction of gamma-aminobutyric acid (GABA)-mediated transmission by a convulsant benzodiazepine. 50 63

In the year May 1976 to April 1977, 489 enquiries about the management of tricyclic antidepressant poisoning received at the London Centre of the National Poisons Information Service were followed-up. One hundred and sixty-four patients (33.5%) were unconscious, convulsions occurred in 62 (12.7%), hypotension in 31 (6.3%), respiratory depression in 28 (5.7%), tachydysrhythmias in 17 (3.5%) and cardiac arrest in 12 patients (2.5%). Sixteen patients died (3.3%). No statistically significant differences were found between individual antidepressants although poisoning with amitriptyline-like drugs resulted in a significantly higher proportion of unconscious patients than poisoning with imipramine-like drugs (P less than 0.01). There were more asymptomatic children than adults and more unconscious adults than children. Tricyclic antidepressant poisoning is a major clinical problem in general medical and paediatric practice.
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PMID:The problem of tricyclic antidepressant poisoning. 51 29

In a prospective study 44 children, aged 6 months to 5 years, admitted to hospital with febrile convulsions or epilepsy, were treated with diazepam in solution administered rectally during 59 generalised attacks. Rectal administration of diazepam was effective in the acute treatment of convulsions in 80% of cases. In 10% the treatment failed, whereas diazepam administered intravenously had prompt effect; another 10% of the convulsions wer resistant to diazepam, irrespective of the route of administration. The therapeutic effect was significantly correlated with the duration of convulsions before treatment started. Early treatment (convulsions less than or equal to 15 minutes) had effect in 96%, and late treatment (convulsions greater than 15 minutes) in 57% of cases. A total of 317 children admitted with febrile convulsions were treated prophylactically with diazepam administered rectally whenever the temperature was greater than or equal to 38.5 degrees C. No case of significant respiratory depression or other serious side effects was observed. The rapid and reliable anticonvulsant effect of diazepam given rectally and the very few side effects makes this treatment a valuable alternative to IV administration in childhood.
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PMID:Rectal administration of diazepam in solution in the acute treatment of convulsions in infants and children. 52 27

Four prototypic anticonvulsants were tested for their effectiveness against barbiturate withdrawal in cats. The effects were evaluated on a total of over 20 motor, autonomic and behavioral withdrawal signs. The animals were made physically dependent by 5 weeks of twice daily "maximally tolerable" sodium pentobarbital dosing intragastrically. Anticonvulsants were administered by intravenous infusion 25 hours after the final dose of chronic pentobarbital treatment when all withdrawal signs had become severe and grand mal type withdrawal convulsions were observed. Phenobarbital blocked withdrawal signs quite effectively at doses that caused no significant acute central nervous system depression. Trimethadione also reversed most withdrawal signs, but some signs persisted even at doses causing overt acute toxicity. Dimethadione was less effective than the parent compound, trimethadione, in reversing withdrawal but caused greater acute toxicity. Phenytoin was in effective for most withdrawal signs and some signs were made worse. The clonic phase of withdrawal convulsions was accentuated and the overall condition of the animals worsened. During withdrawal, the animals were less sensitive (tolerant) to phenobarbital but were more sensitive to acute toxicity from the other drugs tested.
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PMID:Evaluation of anticonvulsants in barbiturate withdrawal. 56 Apr 73

Complexes formed by hematoporphyrin with donor molecules were prepared and isolated. Among these complexes particular attention is given to that formed by reacting dimethylaminoethanol with hematoporphyrin. Some data are reported on the chemical evidence of formation like u.v. spectra. The product, named Hematodeanol, determines some sufficiently specific effects on the CNS; it remarkably cuts down the depression induced by pentobarbital, moderately hinders convulsions by metrazole, delays hypothermia by reserpine, facilites the learning of conditioned avoidance response (CAR) and improves the learning of a sound discrimination at variable interval. The actions become evident when tests are carried out after a continuous treatment for 7 days and according to the data of the investigation of pharmacokinetic kind, the phenomenon may be attributed to the fact that the drug concentration in the nervous tissue, when it is administered several times at intervals of 24 h, inclines to increase progressively.
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PMID:Charge-transfer complexes of hematoporphyrin having a pharmacological interest. 57 64

The toxic effects of alpha-d-propoxyphene (P) and its primary metabolite alpha-d-norpropoxyphene (NP) were compared to intravenous infusions (100 min.) of equimolar doses of P and NP (80 micronmol/kg equivalent to 30 mg/kg P HCl) in conscious rabbits. During P infusion severe respiratory depression and convulsions were seen in all animals, and six of the nine animals died. During NP infusion, however, only minimal respiratory depression was seen and all the animals survived. Considerable prolongation of the QRS complex and cardiac arrhythmias like intermittent A-V block and ventricular extrasystoles were seen in the ECG during both P and NP infusion, while the arterial blood pressure was unchanged. In P injection experiments (6 mg/kg P HCl), ECG changes preceded reduction in respiratory rate and during NP infusion only minor changes were seen in arterial blood gases, demonstrating that the ECG changes produced by P and NP are independent of respiratory depression. The ECG changes were found to be similar to those reported in quinidine intoxication. The QRS prolongation was markedly correlated with plasma concentrations during and after P and NP infusion. The results of the present investigation favour the hypothesis that the contribution of NP to the toxicity of oral P overdosage in man is ascribed to its cardiotoxic action whereas P is responsible for the CNS toxicity (respiratory depression and convulsions) as well as cardiotoxicity.
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PMID:Cardio-respiratory toxicity of propoxyphene and norpropoxyphene in conscious rabbits. 58 Mar 45

Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.
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PMID:Electrocardiographic observation on goats with urea-ammonia poisoning and a consideration on the main cause of death. 60 86

Three cases of neonatal acute retention were associated with convulsions and heavy sedation. Inhibition of micturition may be due to diazepam-induced depression of the nervous system, in association with other anticonvulsants drugs.
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PMID:Retention of urine in the neonate possibly due to anticonvulsant drugs. 60 78


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