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)

In rats, a secretin (Jorpes) intravenous infusion superimposed on an intracolonic sodium acetate perfusion elicits, with respect to control values, a significant depression of Na+ absorption (0.16 mEq./h-0.00 mEq./h.) and mucus secretion (230-40 mg.). When the hormone is superimposed upon an intracolonic infusion of acetic acid, mucus secretion is also significantly inhibited (790-340 mg.). The influence of secretin on organic anion movement was pH related. At pH values of 7.0, absorption was unchanged (0.34--0.33 mEq./h.), at pH values of 2.9, absorption was significantly reduced (0.67-0.41 mEq./h). The secretin impairment of colonic mucus secretion could influence the transport of watersoluble (Na+) and lipid soluble (acetic acid) substances, probably through changes at the "unstirred layer" level.
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PMID:Does secretin influence rat colonic absorption and secretion? 3 Oct 88

It has been demonstrated that L-3hydroxy-6-oxo-N-cyclopropylmethylmorphinan methansulfonate (20681-S) and L-3,14-dihydroxy-6-oxo-N-cyclopropylmethylmorphinan methansulfonate (20682-S), have antinociceptive and narcotic antagonistic properties. In the rodent antinociceptive test, the action of 20681-S was more potent and of longer duration than that of morphine and of cyclazocine after subcutaneous or oral administration. The antinociceptive effect of 20682-S ranked between that of morphine and that of pentazocine in the mouse acetic acid-writhing test. Both compounds possessed potent narcotic antagonistic activities, 20682-S being more active than naloxone and oxilorphan and 20681-S being equipotent with cyclazocine. The latent side effects (respiratory depression and fall in blood pressure) and the acute toxicity of 20681-S and 20682-S, were less than those of reference narcotic antagonists or of narcotic antagonist analgesics.
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PMID:The pharmacology of 20681-S and 20682-S, 6-oxo-N-cyclopropylmethylmorphinans, as narcotic antagonist analgesics. 4 19

Rats given quipazine (5 mg/kg) or LSD (0.05 mg/kg), were decapitated at the time of maximum of behavioral effect of drugs (head twitches), resp. 30 and 15 min, or when the behavioral effects disappeared (resp. 60 and 30 min), and concentrations of dopamine (DA), noradrenaline (NA), serotonin (5HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed in the striatum. Quipazine significantly elevated the DA level at both periods tested. LSD at the peak of its action depressed the level of 5-HIAA, and in the next period produced a significant depression of striatal levels of NA, 5HT and 5-HIAA.
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PMID:The effect of quipazine and LSD on monoamines in the rat striatum. 9 44

An uncontrolled clinical trial with 10 depressed patients was conducted to identify the psychopathological symptoms which may be affected by nomifensin administration, and to reveal the possible adverse effects of the drug. Consistent statistically significant improvement was noted in the course of the clinical trial on all of the assessment instruments used, and - with the exception of one patient - all improved while receiving nomifensin. Most of the therapeutic changes were seen within the first three weeks of treatment, and they included improvements of depression, as well as of hostility, a symptom which usually remains unaffeCTED BY TRICYclic antidepressant drugs. To verify the favorable therapeutic effects of nomifensin in depressed psychiatric patients, a standard-controlled clinical trial is in progress; and to verify the action mechanism of nomifensin, a study employing the probenecid technique and the measurement of spinal homovanillic acid (HVA) and 5-hydroxyindole acetic acid (5hiaa) concentration is planned.
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PMID:A clinical trial with nomifensin, a new antidepressant drug. 12 27

Marked depression of locomotor activity was observed in writhing mice given acetic acid i.p. This depression of the activity was evidenced by a squatting posture in reaction to pain. The hypoactivity was reversed dose-dependently by nonnarcotic analgesics such as acetyl-salicylic acid, aminopyrine and mefenamic acid in smaller dosages than those obtained by the conventional writhing syndrome test, and was also reversed dose-dependently by narcotic analgesics such as morphine, pethidine and codeine. Consequently, this hypoactivity test proved to be useful for analgesics screening.
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PMID:A test for analgesics as an indicator of locomotor activity in writhing mice. 54 56

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.
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PMID:Acetate fails to reverse myocardial depression in dogs anesthetized with halothane. 56 99

Effects of beta-(p-chlorophenyl)-GABA (baclofen), a muscle relaxant, on the response of mice and rats to various noxious stimuli were studied. In mice, 5 approximately 10 mg/kg i.p. of baclofen delayed the response time to tail-pinch and hot-plate stimuli but the relaxation was also apparent with this dose range. Mephenesin also delayed the response time to tail-pinch stimuli with the dose producing muscle relaxation. Baclofen, 3 mg/kg i.p., while producing no muscle relaxation, suppressed the acetic acid-induced writhing. The same effect, suppression of writhing and no muscle relaxation, was achieved with 50 mg/kg i.p. of mephenesin. In rats, baclofen (5 approximately 10 mg/kg i.p.) increased the response threshold in Randall-Selitto method and suppressed the bradykinin-induced symptoms, however, muscle relaxation was also produced with these same doses. Increase in response threshold in Randall-Selitto method was achieved with the dose of mephenesin producing muscle relaxation. The time courses of the depression of response to noxious stimuli and the muscle relaxation induced by baclofen and mephenesin were consistent in mice and rats. A small dose (3 mg/kg i.p. in mice, 2 mg/kg/h s.c. in rats) of baclofen reduced the antinociceptive effect of morphine but a larger dose (5 mg/kg i.p. in mice, 7 mg/kg/h s.c. in rats) of baclofen increased or did not alter the effect of morphine. It seems likely that the antinociceptive effect of baclofen may be nonspecific to analgesia.
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PMID:[Effects of beta-(p-chlorophenyl)-GABA (baclofen) on response to noxious stimuli (author's transl)]. 59 82

The presence of a cardiodepressant factor of pancreatic origin has been reported in the plasma of experimental animals and man in a variety of shock states. It has been suggested that the depression of developed tension of the isolated cat papillary muscle may be caused by excess NaCl in the bathing medium rather than a specific cardiodepressant peptide. Incubated pancreatic homogenate was used as a source of this factor, and after protein precipitation, ultrafiltration (10,00 and 1,000 MW), dialysis and lyophilization, the residue was applied to a Sephadex G-10 column in order to ensure the removal of all salts. The protein effluent of the Sephadex column contained all the cardiodepressant activity of the filtered, dialyzed pancreatic homogenate and none of the salt content. To further isolate this cardiodepressant factor, the active residue was applied to a cellulose column and eluted with butanol: glacial acetic acid: water (25:26 v/v/v). This elution gave 8 distinct peptide peaks, one of which, peak 4, contained significant depressant activity. Thus, a cardiodepressant peptide of approximately 250-1,000 MW exists in pancreatic homogenates and this compound is not excess NaCl in the assay system.
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PMID:The chemical nature of a pancreatic cardiodepressant factor. 92 11

A peptide material with opiate-like activity in the guinea-pig ileum was extracted from porcine pituitaries using a hot glacial acetic acid extraction method and was partially purified by gel filtration. When injected intraventricularly in rats, these purified peptides induced strong analgesia, catelepsy, respiratory depression and other opiate-like effects, which lasted for several hours.
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PMID:Porcine pituitary peptides with opiate-like activity: partial purification and effects in the rat after intraventricular injection. 103 19

Phenelzine (PLZ), a nonselective monoamine oxidase inhibitor, is widely used in psychiatry for the treatment of panic disorder and depression. The effects of chronic (28-day) administration of PLZ (0.05 mmol/kg/day) and its N-acetylated analogue, 1-acetyl-2-(2-phenylethyl) hydrazine (N2-acetylphenelzine; N2AcPLZ; 0.10 mmol/kg/day), on alpha 2-adrenoreceptor function were investigated by use of a behavioral test on days 21 and 22. Rats treated with PLZ or N2AcPLZ displayed a significant attenuation of the suppressant effects of clonidine on spontaneous locomotor activity, compared with controls; these results suggest a reduced sensitivity of alpha 2-adrenoreceptors. By day 28, both PLZ and N2AcPLZ had produced greater than 85% inhibition of monoamine oxidases A and B in the brain, heart, and liver. Both drugs induced significant elevations of whole-brain levels of noradrenaline, 5-hydroxytryptamine, and dopamine, compared with those in controls. The levels of acid metabolites of dopamine and 5-hydroxytryptamine (homovanillic acid, 3,4-dihydroxyphenylacetic acid, and 5-hydroxyindole-3-acetic acid) were significantly reduced in both groups of drug-treated animals.
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PMID:Chronic administration of the antidepressant-antipanic drug phenelzine and its N-acetylated analogue: effects on monoamine oxidase, biogenic amines, and alpha 2-adrenoreceptor function. 138 93


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