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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long Sleep (LS) and Short Sleep (SS) mice were used in this study to investigate the interaction between ethanol and taurine. Sleep time (hypnosis) was selected as an index of ethanol-induced central nervous system depression. In order to achieve a similar degree of central nervous system depression with ethanol, SS and LS mice received 5.3 and 3.0 g/kg, IP, of ethanol, respectively. When taurine (7.5, 15 and 25 mumol/kg) was administered intracerebroventricularly (ICV) to LS and SS mice immediately after regaining the righting reflex following ethanol injection, a return to sleep time was produced. This effect of taurine was immediate in onset and occurred in a dose-dependent fashion. LS mice exhibited a greater effect from taurine administration than SS mice. In another experiment LS and SS mice were given ICV TAG, a taurine antagonist (6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide HCl), which significantly reduced the effect of taurine to produce a return to sleep time in the presence of ethanol. TAG did not affect ethanol-induced sleep time. In control experiments, in the absence of ethanol, neither taurine (25 mumol/kg, ICV) nor TAG (1 mumol/kg, ICV) caused a significant loss of the righting reflex (sleep time). When pentobarbital (50 mg/kg, IP) was injected instead of ethanol in the sleep time experiments, taurine (7.5, 15 and 25 mumol/kg, ICV) produced a return to sleep time in LS and SS mice that resembled the effect of taurine with ethanol in SS mice. These results indicate that taurine (ICV) can enhance the central depressant action of ethanol and pentobarbital and that the greatest effect of taurine occurred with LS mice in the presence of ethanol. It is possible that taurine may have some role in the central nervous system depressant properties of ethanol.
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PMID:Effect of taurine on ethanol-induced sleep time in mice genetically bred for differences in ethanol sensitivity. 325 Dec 49

The cardiovascular effects of N-(3,4-dimethoxyphenethyl)-2-(3,4-dimethoxyphenyl-N-methyl-m-dithiane-2- propylamine-1,1,3,3-tetraoxide HCl (tiapamil, Ro 11-1781, Larocord), a new calcium entry blocker, were investigated in chronically-instrumented conscious dogs and compared with those of verapamil and nifedipine. Oral administration of tiapamil to normotensive dogs dilated preferentially the arterial vascular bed as evidenced by marked increases in the coronary and abdominal aortic blood flow in the absence of a depression of the myocardial contractile force. The vasodilator effects induced a reflex increase in heart rate and cardiac output, which prevented a decrease in blood pressure in normotensive, but not in renal hypertensive dogs. By contrast, verapamil and nifedipine decreased blood pressure in both normotensive and renal hypertensive dogs. At equieffective vasodilating doses, a negative inotropic effect was not seen with tiapamil. By contrast, nifedipine caused a marginal fall and verapamil a marked decrease in myocardial contractile force. This favourable pattern of hemodynamic properties makes tiapamil appear to be a useful agent for the treatment of hypertension and angina pectoris.
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PMID:Cardiovascular effects of three calcium entry blockers in conscious dogs. 343 96

Effects of dietary supplementation of thiamin-HCl (1 g daily) and a feed grade double sulfate of magnesium and potassium (Dynamate, added at 1.8% of diet dry matter; referred to as sulfate) on ruminal passage of thiamin and site of digestion in dairy steers (464 kg initial weight) fed a 77% concentrate diet were determined in a 4 X 4 Latin square experiment. Sulfate supplementation tended to reduce duodenal thiamin flow with (P less than .08) and without (P greater than .10) added thiamin. Supplementation with thiamin alone decreased ruminal disappearance of fed organic matter and nitrogen (P less than .03) and total tract disappearance of starch (P less than .06) and nitrogen (P less than .02), and increased ruminal microbial efficiency (P less than .04). Sulfate addition to the high thiamin diet alleviated these effects but depressed microbial efficiency (P less than .05). Sulfate included in the diet without added thiamin affected plasma thiamin positively, whereas sulfate added to the diet with supplemental thiamin changed plasma thiamin negatively (interaction, P less than .06). In conclusion, a marked depression of ruminal digestion induced by dietary thiamin-HCl supplementation disappeared upon dietary addition of sulfate and sulfate depressed the quantity of thiamin passing from the rumen. Because preventing thiamin deficiency and optimizing site of digestion in feedlot cattle are desired, these changes deserve further study.
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PMID:Effects of supplement sulfate (Dynamate) and thiamin-HCl on passage of thiamin to the duodenum and site of digestion in steers. 345 20

Propranolol HCl (7.5 mg X kg-1), timolol maleate (7.0 mg X kg-1), and sotalol HCl (10 mg X kg-1) were administered intracerebroventricularly (icv) to spontaneously breathing (SB) rats. The respiratory rate declined until the rats all died from respiratory arrest. Artificial ventilation resulted in survival of the rats for a 3-hr observation period. Intravenous (iv) administration of the same doses of the three beta blockers to SB rats did not result in either respiratory depression or death. Except for a decrease in heart rate (HR) the hemodynamic and respiratory parameters remained almost constant during the 3-hr observation period after iv administration to SB rats. After icv administration to SB as well as to ventilated rats no significant differences could be observed in the initial decrease in HR in comparison with iv administration. In SB rats at the end of the experiments a further decrease in HR was observed which might be ascribed to hypoxia since it did not occur in ventilated rats. After icv administration of each drug to the ventilated rats, mean arterial blood pressure showed a significantly greater decrease at the end of the 3-hr observation period than after iv administration. Plasma concentrations of the three drugs were determined just before death after icv administration in SB rats. In the other two groups they were measured at mean survival time and at the end of the experimental period. The plasma concentrations showed that the route of administration rather than the concentration of the beta blocker in plasma determines the occurrence of respiratory arrest. It was concluded that an overdose of propranolol, timolol, or sotalol can cause a centrally mediated respiratory arrest. Furthermore, a central mechanism appears to be implicated in the decrease in blood pressure.
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PMID:Central origin of respiratory arrest in beta-blocker intoxication in rats. 360 68

In male Swiss-Webster mice sleep time (hypnosis) was used as an index of ethanol-induced central nervous system depression. Ethanol (4 g/kg, IP) was administered to animals and the onset to sleep time (loss of the righting reflex) and the duration of sleep time were recorded. At the end of the ethanol-induced sleep time, taurine (7.5, 15 or 25 mumol/kg, ICV) was injected. Immediately after the ICV injection of taurine the mice again lost the righting reflex. This effect of taurine occurred in a dose-dependent fashion. In the absence of ethanol, taurine (25 mumol/kg, ICV) did not produce a significant sleep time. In another experiment when TAG, 6-amino-methyl-3-4H-1,3,4-benzothiadiazine-1,1-dioxide HCl, (a taurine antagonist) was given to mice, TAG (0.9 mumol/kg, ICV) significantly reduced the effect of taurine (7.5, 15 and 25 mumol/kg, ICV) to reinstate a sleep time in the presence of ethanol. TAG, however, did not alter ethanol-induced sleep time. These results indicate that taurine (ICV) can enhance the central depressant action of ethanol and that this effect of taurine can be attenuated by TAG. The antagonism of taurine by TAG appears to be noncompetitive in nature.
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PMID:Ethanol-induced sleep time: interaction with taurine and a taurine antagonist. 362 38

Cardiovascular effects of (2''R)-4'-O-tetrahydropylanyladriamycin X HCl (THP) and doxorubicin (adriamycin, ADM) were studied in hamsters. In experiments to observe acute effects, THP was administered intravenously at a dose of 12.5, 25.0 or 50.0 mg/kg, and ADM at 1.56, 3.13 or 6.25 mg/kg was given to different subjects. The THP caused slight ECG alterations at a dose of 12.5 mg/kg. At a dose of 25.0 mg/kg or 50.0 mg/kg, THP caused moderate to remarkable alterations in ECG like a widening of PR and PRc interval, A-V block, ST segment depression and T wave flattening. The ADM caused moderate to remarkable alterations in ECG at a dose of 3.13 mg/kg or 6.25 mg/kg, including arrhythmia, bradycardia, A-V block, ST segment changes and T wave flattening. These changes caused by THP and ADM recovered within 5 approximately 10 minutes after injection. Alterations in the ultrastructure of the myocardium caused by THP at a dose of 50.0 mg/kg included some cells with slight changes like swelling of mitochondria, focal intracellular edema, and enlargement of myofibrils. The ADM, at a dose of 3.13 mg/kg, induced severer swelling of mitochondria than THP, dilatation of sarcoplasmic reticulum, intracellular edema, and disorganization of myofilaments. At a dose of 6.25 mg/kg of ADM, these changes became more pronounced. In experiments to observe subacute effects, hamsters were treated with THP or ADM by daily intraperitoneal injections for 15 consecutive days, and then allowed to be recovered for 15 days. Dose levels of THP or ADM were 0.125, 0.25, 0.5 and 1.0 mg/kg. General toxicity, ECG, hematological and blood biochemical analysis, and electron microscopic examination were studied. In the ECG study, THP-treated hamsters showed a reversible elevation of R wave amplitude at a daily dose of 0.5 mg/kg. Widening of PR and PRc interval, elevation of R and S wave amplitude, and reduction of T wave amplitude were observed at a daily dose of 1.0 mg/kg of THP. Hamsters treated with ADM showed increase of heart rate, reduction of T wave amplitude, and shortening of PR and PRc interval at a daily dose of 0.5 mg/kg. Severe changes were observed at a daily dose of 1.0 mg/kg of ADM including an increase of heart rate, elevation of R wave amplitude, reduction of S and T wave amplitude, and shortening of QT interval. The electron microscopic examination revealed that THP-treated hamsters showed separation of intercalated discs, formation of myelin structure, and dilatation of T-tubules at a daily dose of 1.0 mg/kg. Similar changes were caused by ADM at a daily dose of 0.25 to 1.0 mg/kg.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Effect of (2"R)-4'-O-tetrahydropyranyladriamycin, a new antitumor antibiotic, on the cardiac function of hamsters]. 371 57

The ability of the kidney to reabsorb bicarbonate is held to be a function of plasma CO(2) tension, carbonic anhydrase activity, and potassium stores. The effects of alterations of extracellular volume on bicarbonate reabsorption were studied in dogs whose arterial Pco(2) was kept constant at 40 mm Hg (range 35-45 mm Hg). The effect of extracellular volume expansion was studied in dogs receiving hypertonic bicarbonate and isotonic saline, isotonic saline alone (two of the animals in this group received HCl to lower the plasma bicarbonate concentration), and isotonic bicarbonate. The results were similar in each group. Extracellular volume expansion depressed bicarbonate reabsorption. This depression was related not to changes in glomerular filtration rate (GFR) or bicarbonate concentration, but to the increase of fractional sodium excretion. In addition, volume expansion with bicarbonate increased chloride excretion. Bicarbonate loading was performed in two groups of dogs in which effective expansion of extracellular volume was minimized by hemorrhage or acute constriction of the thoracic vena cava. Both groups demonstrated enhanced bicarbonate reabsorption relative to that seen in the volume-expanded groups. Release of the caval ligature promptly decreased bicarbonate reabsorption. Plasma potassium decreased in all animals studied, but the changes in bicarbonate reabsorption noted could not be related to the decrease. This study demonstrates that the state of effective extracellular volume is a major determinant of bicarbonate reabsorption by the kidney.
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PMID:Regulation of renal bicarbonate reabsorption by extracellular volume. 541 84

In a patient with myasthenic syndrome neuro-muscular transmission was characterised by depression and facilitation. The relative extent of these two processes varied between muscles, and in the one muscle with time. Guanidine HCl treatment corrected the electrophysiological defect. Oral choline increased muscle action potential amplitude in response to single shocks. Intravenous choline produced features indicating cholinergic autonomic stimulation. Pimozide and plasmapheresis had no effect. Animal in-vivo and in-vitro studies performed to detect a circulating factor which interferes with neuro-muscular transmission were negative.
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PMID:Myasthenic syndrome: effect of choline, plasmapheresis and tests for circulating factor. 611 Jul 9

The effects of clomipramine HCl (15 mg kg-1 i.p.) on behaviour, body temperature and brain amines were investigated in rats that had been chronically treated twice daily with increasing doses of delta 9-tetrahydrocannabinol (delta 9-THC, 2-6 mg kg-1 i.v.). delta 9-THC produced a biphasic change in behaviour, stimulation followed by depression, and a pronounced hypothermia. Tolerance developed rapidly to these effects of delta 9-THC. Chronic treatment with delta 9-THC reduced the levels of homovanillic acid, 5-hydroxytryptamine and noradrenaline. The level of dopamine was not altered with chronic treatment and tolerance appeared to develop to the increased levels of 5-hydroxyindoleacetic acid induced by delta 9-THC. Injection of clomipramine, 12-14 h after 2, 5 or 10 days of delta 9-THC treatment induced characteristic changes in the rats behaviour which consisted of writhes, backward kicking, wet shakes, jumps ataxia and front paw and whole body tremor. The severity of the behavioural changes appeared to be dependent on the period of delta 9-THC administration and they were not accompanied by a change in body temperature or consistent changes in brain amines or metabolites. The results indicate that physical dependence on delta 9-THC may occur since clomipramine is able to precipitate changes in behaviour, indicative on an abstinence syndrome, in rats chronically treated with delta 9-THC. It is suggested that tryptaminergic mechanisms are altered during chronic delta 9-THC treatment and that clomipramine induces the behavioural changes by interacting with an altered tryptaminergic system.
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PMID:Time-course of the effects of chronic delta 9-tetrahydrocannabinol on behaviour, body temperature, brain amines and withdrawal-like behaviour in the rat. 612 98

The rat taste cells responded to the four basic taste stimuli (0.5 M NaCl, 0.02 M quinine-HCl (Q-HCl), 0.01 M HCl and 0.5 M sucrose) with depolarizing or hyperpolarizing receptor potentials. The rates of obtaining hyperpolarizing responses under 41.1 mM NaCl adaptation were 3% for NaCl, 42% for Q-HCl, 21% for HCl and 37% for sucrose. Most of the taste cells responded to more than two kinds of taste stimuli. The ratio of mean magnitudes of depolarizing and hyperpolarizing responses for the four basic taste stimuli under 41.4 mM NaCl was as follows: NaCl:Q-HCl:HCl:sucrose = 100:9:48:2. The ratio of mean magnitudes of tonic chorda tympani nerve responses for the four basic taste stimuli under 41.4 mM NaCl was: NaCl:Q-HCl:HCl:sucrose = 100:5:37:2. Comparison of both taste cell and nerve responses suggests that the depolarization of a taste cell is concerned with a generation of gustatory neural impulses, and that the hyperpolarization is concerned with a depression of the impulses.
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PMID:Dependence of gustatory neural response on depolarizing and hyperpolarizing receptor potentials of taste cells in the rat. 613 31


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