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)

Combined investigation in patients with maniac-depressive psychosis revealed the close relation of depression to the direction in which changes of central and peripheral links of bodily neurohumoral system occur. With even some of the homeostatic functions normalized as a result of an adaptogenic effect of hormonal and biologically active drugs (triiodothyronine, thyrotropin, insulin, Sodium succinate, pituitrin (vasopressin), somatotropin, retabolil), the depressive affect weakened or disappeared. Combined therapy of depression is recommended comprising antidepressants and some hormonal drugs promoting the adaptation processes of the body.
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PMID:[Effect of various biologically active substances and hormonal preparations on the pathogenetic mechanisms of manic-depressive psychoses]. 306 42

A 5 years old girl with status epilepticus refractory to treatment with Diphenylhydantoin at a dose of 30 mg/kg/day and Thiopental in continuous IV perfusion at a dose of 4 mg/kg/h is presented. Control of status was achieved by continuous IV perfusion of Chlormethiazole at a dose of 10 mg/kg/h which also caused respiratory depression. Seizure activity reappeared after IV perfusion of Chlormethiazole was retired, and could be controlled only with Sodium Valproate. Mechanisms of action of Chlormethiazole and its effectiveness in treatment of refractory status epilepticus are revised.
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PMID:[Treatment of refractory status convulsivus with chlormethiazole]. 314 89

Lithium salts, in particular the carbonate and citrate, were formerly in widespread use, forming part of alkaline salt mixtures which were used for treatment of the many disorders belonging to the uric acid diathesis. Among these disorders were mania, depression, acute mania, acute melancholia and periodic depression. Satisfactory prophylactic effects on periodic depression were directly claimed. Daily doses of 3 to 26 mmol of lithium were recommended as standards. Only slight or moderate symptoms of poisoning were reported in a very few cases during the period in question (1860 to 1930), when the popularity of these lithium-containing prophylactic drugs with a favourable therapeutic index was at its peak. Lithium intoxication was not a serious clinical problem until 1949 when Cade introduced his fortuitously effective, but nevertheless high, dosage regimen which was continued until signs of recovery from mania appeared. For the maintenance dose, Cade in principle recommended, but seldom adhered to, 17 mmol/day. Chronic lithium intoxication starts insidiously with silent affliction of the kidneys followed by 'prodromal' symptoms, and when moderate severity has been reached, an accelerating renal vicious circle with decreasing kidney function is imminent. After this point the chronic intoxication resembles acute intoxication. Active detoxification at this, or an earlier stage, leaves the patient with a good chance of recovery. At a later stage, with the occurrence of oliguria, semi-coma or coma, and latent convulsive movement, recovery is less certain. There is no specific antidote for the toxic effects of lithium. Haemodialysis is the most effective treatment for acute lithium poisoning. For patients with impaired, or potentially impaired renal function, peritoneal dialysis may be an alternative, but less effective, treatment. Forced diuresis demands unimpaired renal function, and is little more effective than withdrawal of treatment, supplemented with correction of water and electrolyte balance. Sodium overloading is not recommended. Patients on lithium prophylaxis are treated on an outpatient basis. Prevention of intoxication depends on cooperation between patient and clinician, and possibly on the use of smaller, low risk dosages in most patients.
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PMID:Clinical features and management of lithium poisoning. 328 25

Sodium selenite was fed in the diet in concentrations of 3, 1 and 0.50 ppm to hybro-type chicks for 4 weeks from the age of 7 d. The chemical's effects on growth and tissues were investigated. One and 3 ppm dietary levels of selenium caused depression of growth, fatty change, focal necrosis, congestion of the sinusoids and slight fibroplasia in the liver, congestion and degeneration and/or necrosis of the cells of the proximal renal tubules and of the cardiac muscle fibers and hemorrhage in the thigh and breast. These changes were accompanied by an increase in the activity of sorbitol and glutamic dehydrogenases (SDH and GDH) and in the concentration of potassium, and a decrease in the levels of total protein, calcium and zinc in the serum. Susceptibility to hemorrhage and damage to kidneys and liver persisted for 3 weeks after the test diet was withdrawn. One-half of 1 ppm-selenite meal produced no adverse effects on the chicks.
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PMID:Effects of various levels of dietary selenium on hybro-type chicks. 370 35

Sodium N-benzyl-D-glucamine dithiocarbamate (NBG-DTC), which was newly synthesized, sodium N-methyl-D-glucamine dithiocarbamate (NMG-DTC), and 2,3-dimercapto-1-propanol (BAL) were evaluated for their efficacy in mobilization of cadmium from the body using rats which had received cadmium, 30 min and 24 h earlier. At both 30 min and 24 h after treatment with cadmium, these chelating agents significantly enhanced the biliary excretion of cadmium, but did not influence the urinary excretion of the metal. Such an enhancement effect of NBG-DTC on the biliary excretion of cadmium was much larger than that of NMG-DTC or BAL. These chelating agents were effective in mobilizing cadmium from the liver at 30 min after pretreatment with cadmium. NBG-DTC showed the largest effectiveness on the depression of cadmium content in the liver. However, the contents of cadmium in the liver and kidney of rats given cadmium, 24 h earlier, did not significantly change at 3 h after treatment with the chelating agents. These results show that the injection of NBG-DTC at both 30 min and 24 h after treatment with cadmium can much more effectively mobilize cadmium from the body mainly through the bile without redistribution of cadmium to tissues than injection of NMG-DTC and BAL.
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PMID:Effects of chelating agents on biliary and urinary excretion and tissue distribution of cadmium in rats. 378 63

To determine whether accumulation of long-chain acyl carnitine contributes to electrophysiological abnormalities induced by hypoxia, we characterized effects of normoxic and hypoxic perfusion on the subcellular distribution of endogenous long-chain acyl carnitine and transmembrane potentials of cultured rat neonatal myocytes. Hypoxia increased long-chain acyl carnitine more than 5-fold. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (10 microM), a carnitine acyltransferase inhibitor, precluded accumulation of long-chain acyl carnitine induced by hypoxia. Tissue was processed for electron microscopy by a procedure specifically developed for selective extraction of endogenous short-chain and free carnitine but retention of endogenous long-chain acyl carnitine. In normoxic-perfused cells, long-chain acyl carnitine was concentrated in mitochondria and cytoplasmic membranous components. Only small amounts were present in sarcolemma. Hypoxia increased mitochondrial long-chain acyl carnitine by 10-fold and sarcolemmal long-chain acyl carnitine by 70-fold. After 60 minutes of hypoxia, sarcolemma contained 1.4 X 10(7) long-chain acyl carnitine molecules/micron 3 of membrane volume, a value corresponding to approximately 3.5% of total sarcolemmal phospholipid. Hypoxia also significantly decreased maximum diastolic potential, action potential amplitude and maximum upstroke velocity of phase 0. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate inhibited accumulation of long-chain acyl carnitine in each subcellular compartment and prevented the depression of electrophysiological function induced by hypoxia. These results strongly implicate endogenous long-chain acyl carnitine as a mediator of electrophysiological alterations induced by hypoxia.
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PMID:The dependence of electrophysiological derangements on accumulation of endogenous long-chain acyl carnitine in hypoxic neonatal rat myocytes. 394 41

1 A technique has been developed for open-ended perfusion of the cerebroventricular system of the unanaesthetized dog.2 Perfusion with an artificial CSF solution containing inulin and (42)K allowed the potassium fluxes out of and into the CSF to be monitored over a period of 2 to 3 hours.3 Sodium thiopentone and sodium pentobarbitone, in doses producing light anaesthesia, caused varying degrees of depression (up to 50%) in the CSF potassium fluxes, influx being consistently more affected than efflux. These effects are attributed to a decrease in the potassium exchange between extracellular and intracellular compartments in the brain.4 Diazepam depressed both potassium fluxes by up to 10% while there was some evidence that diphenylhydantoin depressed only potassium influx.5 Paraldehyde, in contrast to the other drugs, when given at a dose level sufficient to produce light anaesthesia, stimulated CSF potassium fluxes, particularly efflux.
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PMID:The effects of certain anaesthetic and anti-convulsant drugs on the CSF potassium fluxes of the dog. 445 7

Twenty-three pigs, 1-3 mo of age, were fitted variously with intraperitoneal, intrajugular, intraportal, and intraduodenal catheters. After a 4-h fast, porcine cholecystokinin (CCK), 5-40 Ivy dog units/kg body wt (IDU/kg); caerulein, 0.25-2 micrograms/kg; or the octapeptide of cholecystokinin (CCK-OP), 5-40 IDU/kg, was given parenterally; or 2-5% sodium oleate or 5% protein hydrolysate (5 ml/kg) was injected intraduodenally. Pelleted feed intake was then measured for 10 min. Food intake was depressed in a dose-related fashion in all instances as compared to after 0.9% NaCl control injections. For example, feed consumption following 5 and 40 IDU/kg of CCK intrajugularly was 84 +/- 2 and 6 +/- 4 (SE) %, respectively, of control intake. Intraportal infusion produced a greater depression of feeding. A conditioned taste aversion could not be formed to CCK, caerulein, or CCK-OP. Sodium oleate or protein hydrolysate, releasers of endogenous CCK, depressed feeding, and this satiety effect was attenuated when given with 0.5% tetracaine. The results support the hypothesis that CCK participates in rapid, presumably preabsorptive, satiety.
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PMID:Cholecystokinin and satiety in pigs. 626 13

The indolalkylamine alkaloid yohimbine induced two phenomenologically-different types of sodium current (INa) inhibition in the voltage-clamped frog node of Ranvier, a tonic and a phasic ('use-dependent') block. The latter developed during a repetitive membrane stimulation with short (5 ms) depolarizing pulses at frequencies at 1 to 10 Hz. Unlike repetitive pulsing, a single-long lasting (1 s) depolarizing step did not produce a phasic block. Turning on a hyperpolarizing prepulse (50 ms to E = -123 mV) immediately before each test pulse produced a gradual unblocking of Na channels, while a depolarizing prepulse (to -86 mV) enhanced the phasic block. Yohimbine blocked the outward INa much more strongly than the inward ones. Reduction of external Na+ ions concentration from 112 to 55 mM caused a shift in the voltage-department of yohimbine block to more negative voltages, which coincided with the shift of INa reversal potential. Sodium current inhibition produced by yohimbine was accompanied by partial depression of the intramembrane charge movements ('ON-response'). Modification of Na channels by batrachotoxin made the Na channels resistant to both tonic and phasic blocking action of yohimbine. The features of the yohimbine-induced block suggest an interaction of the drug with open Na channels. The current-dependence of yohimbine block indicates an electrostatic interaction between Na+ ion and charged (protonated) form of yohimbine within the channel lumen and suggests the localization of the receptor at the inner mouth of the channel. Binding of yohimbine to the channel receptor promotes the inactivation of this channel. Comparison of the effects of yohimbine on NA and gating currents with those of local anesthetics leads us to suggest that these drugs share a common receptor.
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PMID:The effect of yohimbine on sodium and gating currents in frog Ranvier node membrane. 628 68

Sodium arachidonate (AA, 1.5 mg/kg) was injected into the coronary arteries in 16 rabbits. Arrhythmia, marked ST-T depression and apnea appeared in all cases, and 7 cases died within 10 min after the AA. Before the injection, the thromboxane B2 (TXB2) value was 1.2 +/- 0.2 ng/ml (mean +/- SE) and the 6-keto-PGF1 alpha value was 2.1 +/- 0.4 ng/ml. Three minutes after the AA, TXB2 values were 5.0 +/- 1.1 in the surviving cases and 17.9 +/- 6.5 ng/ml in the cases which died. 6-keto-PGF1 alpha values were 47.7 +/- 4.6 in the surviving cases and 248.5 +/- 69.3 ng/ml in the cases which died. There occurred no deaths in 7 cases pretreated with aspirin (ASA) and in 11 cases pretreated with OKY-046 and 1581, which are specific inhibitors of TXA2 synthetase. TXB2 values did not change in the ASA and OKY groups after the AA injection. 6-keto-PGF1 alpha values did not change in the ASA group and increased in the OKY group after the AA injection. Histological findings of the heart showed more remarkable ischemic changes in the non-pretreated group than in the ASA and OKY groups. These results suggest a role for TXA2 in sudden death. PGI2 production was extremely enhanced, suggesting the presence of a protective mechanism against thrombogenesis in vivo.
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PMID:Sudden death induced by intracoronary platelet aggregation. 640 15


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