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

The s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection, the marked sedative response to morphine was restored, suggesting that the morphine-induced decrease in SLMA of rats may depend on the release of 5-hydroxytryptamine by morphine. By contrast, the s.c. administration of 5 mg/kg of morphine-HCl produced a significant increase in SLMA of rats. The magnitude of the increase was reduced by atropine, scopolamine or alpha-methyl-p-tyrosine. It appears that both adrenergic and cholinergic mechanisms participate in the increase in SLMA of rats induced by morphine. Both the increase in SLMA produced by 5 mg/kg of morphine and the decrease in SLMA induced by 20 mg/kg of morphine were completely antagonized by the s.c. administration of naloxone-HCl, 0.0625 and 0.25 mg/kg, respectively. Thus, it appears that the receptor with which morphine interacts to produce stimulation is chemically identical with or very similar to the receptor with which morphine combines to induce depression. The former receptors, however, are likely to be located on different neurons from the latter.
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PMID:Effects of humoral modulators and naloxone on morphine-induced changes in the spontaneous locomotor activity of the rat. 0 52

The effect of adrenergic blockade on gastric secretion altered by catecholamines was studied for 4 hr after injection in rats with chronic gastric fistulas. The alpha-adrenergic blockers phenoxybenzamine and phentolamine significantly inhibited the basal secretion of HCl and pepsin. Blockade of the beta-adrenergic receptors with propranolol did not change this secretion. Practolol in small doses slightly increased and in larger doses inhibited HCl out-put. Of the catecholamines, adrenaline and dopamine most markedly reduced HCl and pepsin secretion, while noradrenaline and isoprenaline had a weaker effect. Neither alpha- nor beta-adrenergic blockers prevented the inhibitory action of the catecholamines employed, but intensified the depression of the gastric secretion provoked by them. Adrenergic blockers inhibited secretion after catecholamines as well as basal secretion. This indicates that these two antagonistic groups of compounds act independently on the mechanism controlling gastric secretion. It is unlikely that this takes place indirectly through changes in the blood supply of the gastric mucosa.
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PMID:Effect of adrenergic blockade on gastric secretion altered by catecholamines in rats. 1 61

Subtetanic contractions of the guinea-pig isolated soleus, a slow-contracting skeletal muscle, were evoked by transmural field-stimulation. Isoprenaline caused a dose-dependent depression of the contractions. This effect was inhibited by propranolol and H 35/25 (1-(p-tolyl-2-isopropylamino-1-propanol) but not by practolol. Similar results were obtained for terbutaline. Tazolol and H 80/62 (1-isopropylamino-3-(p-hydroxyphenoxy)-2-propanol (HCl), selective beta1-agonists, had no effect per se but inhibited the effect of terbutaline. Adrenaline, noradrenaline, and dopamine all caused a dose-dependent decrease in the force of the soleus contractions, their potencies being in that order. Tyramine did not appreciably affect the contractions nor did it inhibit the effect of terbutaline. Pretreatment with reserpine, if anything, increased the response to terbutaline. It is concluded, in conformity with previous in vivo studies, that the adrenergic receptor mediating the effect on the soleus muscle contractions is of the beta2-type. Indirect sympathomimetic effects do not contribute to the responses observed on the isolated soleus muscle.
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PMID:Analysis of the beta-receptor mediated effect on slow-contracting skeletal muscle in vitro. 2 Dec 60

The addition of d-amphetamine to morphine has been reported to result in an increase of analgesic potency in experimental animals and man, but no data on the toxicity of such combinations are available. This study is intended to provide systematic information on the toxicity, analgesic potency and degree of physical impairment (swimming endurance) of a combination of 12 mg morphine sulfate with 10 mg d-amphetamine HCl per ml which is now under clinical investigation. Mice were used as experimental subjects. Meperidine, methadone and pentazocine were substituted for morphine using clinically equally analgesic doses and keeping the d-amphetamine amount constant. The toxicity of all analgesics especially that of morphine was enhanced in the combination, least so in the case of meperidine. The degree of increase of analgesic power by the addition of d-amphetamine was greatest with morphine and quantitatively in satisfactory agreement with present clinical experiences. However, the relationship between the increases of toxicity and of analgesia is not necessarily most favorable for this drug. For the other three analgesics increases in toxicity and analgesia were more in line, meperidine showing the best ratio. Swimming endurance was decreased with full analgesic doses of all four compounds. The presence of d-amphetamine tended to reverse this depression. The data were analyzed in relation to their possible predictive value for the use of such combinations in man for the therapeutic dose range and in the event of overdosage.
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PMID:A study of the effect of d-amphetamine on the toxicity, analgesic potency and swimming impairment caused by potent analgesics in mice. 24 3

1. Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell & Mostaghni, 1975).2. When 60 mM-HCl was infused into the duodenum, gastric emptying was arrested but both acid and pepsinogen secretion continued at a low level. Duodenal infusion with isotonic NaHCO(3) caused rapid exponential emptying of the test meal and acid and pepsinogen output was more than doubled.3. Duodenal infusion of amino acids in isotonic NaHCO(3) did not affect the rapid emptying, except infusion with tryptophan, which caused a measureable degree of inhibition of emptying, with concomitant effects on acid and pepsinogen secretion4. Tryptamine and 5-hydroxytryptamine (5-HT) incorporated in low concentration into isotonic NaHCO(3) also produced depression of gastric emptying, acid and pepsinogen levels comparable to the response initiated by acid infusate. Tryptophan was effective only in non-physiological amounts while 5-HT and tryptamine were active in smaller doses.5. Our results suggest that the inhibition of gastric emptying following duodenal infusion of tryptophan noted by Stephens, Woolson & Cooke (1975) may be due to the duodenal synthesis of its biogenic amine derivatives tryptamine and 5-HT.6. The level of activity of the three gastric functions, emptying, acid secretion and pepsinogen secretion appears to be linked. A single stimulus, therefore, could evoke a duodenal receptor or receptors to mediate or suppress activity of the gastric smooth muscle and secretory cells through interrelated mechanisms. The effect of some duodenal infusates, however, produces some variability in response which suggests differential activation of different receptors with consequent variable motor activity on effector cells.
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PMID:Gastric emptying and secretion in the calf on duodenal infusion of tryptophan, tryptamine and 5-hydroxytryptamine. 48 Feb 33

In an attempt to circumvent the complexities of systemically administered ethanol and tetrahydroisoquinolines (TIQs), iontophoresis and micropressure application were used to test these agents in single rat neurons. Alcohol applied by either method depressed cerebellar Purkinje cells in a concentration-dependent, non-specific, local anesthetic-like manner. Tests of tetrahydropapaveroline.HCl (THP) on neurons from three brain areas also showed depression of spontaneous discharge, although, in contrast to ethanol, little or no local anesthetic-like action was observed, and at equivalent ejection currents or pressures, the THP depressions appeared to be more pronounced. The underlying mechanisms for these responses are unknown.
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PMID:Central neurons are depressed by iontophoretic and micropressure application of ethanol and tetrahydropapaveroline. 52 79

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

Experiments were conducted with immature rats fed L-amino acid purified diets varying in total N and arginine. The experiments demonstrated that total N intake was the factor responsible for increased orotic acid excretion during arginine deficiency. Increased orotic acid excretion was accompanied by increased liver transaminase activities and increased liver concentrations of NH4-N and glutamine. Arginine requirements for growth and normal metabolite excretion increased as dietary N was increased. Accompanying elevated urinary citrate during N deprivation and arginine deficiency was a depression of liver isocitrate dehydrogenase activity. Citrate excretion was lower if arginine was fed as the HCl compared to the free base. During a partial or total arginine deficiency citrate excretion was elevated at varying dietary N concentrations. Urinary pH was not significantly changed by level of dietary N or arginine.
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PMID:Dietary protein intake and arginine requirements in the rat. 62 13

In unanesthetized spinal cats, clonidine HCl (5-50 microgram/kg, i.v.) rapidly and markedly depressed excitatory transmission through two spinal pathways to sympathetic preganglionic neurons. Depression through either pathway was dose-dependent and persisted for more than 3 hr but could be rapidly antagonized at any stage by tolazoline HCl in a dose-ratio of about 1:100. The two spinal pathways were also depressed transiently by L-dopa and for prolonged periods by 5-HTP; both precursors were shown to act by releasing 5-HT from bulbospinal 5-HT terminals and their depressant effects were also antagonized by tolazoline. In the absence of 5-HT-induced depression, L-dopa only enhanced transmission through both pathways by inducing release of catecholamines from bulbospinal NE terminals. These results indicate that clonidine depresses sympathetic activity by stimulating inhibitory 5-HT receptors on sympathetic preganglionic neurons, a mechanism that adequately accounts for its central vasodepressor effect.
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PMID:Depression of sympathetic preganglionic neurons by clonidine: evidence for stimulation of 5-HT receptors. 75 44

Adult male rats receiving 5 or 20 mg/kg heroin HCl by single injections (08:00 or 20:00 hr) or in 3 equal injections (8 hr intervals) showed a disruption in the normal diurnal pattern of behavior. Initially, heroin abolished feeding for several hr after the injection, reduced the total daily food consumption in a dose-related manner, due primarily to decreased night-time feeding, and prevented or slowed weight gain. Subsequent heroin injections led to a phase of vigorous feeding following the period of depression. Magnitude and duration of the depression decreased, but the stimulatory phase of feeding became more pronounced as tolerance developed. Total daily food intake and body weight returned towards control levels, but the proportion eaten during daylight hr became elevated. Sporadic feeding occurred on the first withdrawal day with abolition of the stimulatory phase which had followed each heroin injection. Subsequently, the normal diurnal pattern of behavior gradually returned. Close measurement of 24 hr food consumption may be a sensitive and valuable measure of the disruptive effects of narcotic analgesics.
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PMID:Disruption of diurnal feeding patterns of rats by heroin. 94 51


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