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Biomedical subjects

E Nowakowska

Publications and source records attributed to E Nowakowska.

At least 37 records · Page 2Linked to original sources
PubMed1989

1-(3-Trifluoromethylphenyl) piperazine (TFMPP) in the ventral tegmental area reduces the effect of desipramine in the forced swimming test in rats: possible role of serotonin receptors.

1-(3-Trifluoromethylphenyl)piperazine (TFMPP), a serotonin1 (5-HT1) receptor agonist, injected i.p. in doses of 0.1 and 0.6 mg/kg, did not modify the immobility time of rats in the forced swimming test but significantly antagonized the effect of a 7 days treatment with 10 mg/kg per day desipramine (DMI). A similar effect was found on infusing 1 and 5 micrograms/microliters TFMPP bilaterally into the ventral tegmental area (VTA). Infusion of 5 micrograms/microliters TFMPP into the nucleus accumbens or into the globus pallidus did not modify the effect of DMI. The effect of 5 micrograms TFMPP infused into the VTA was prevented by the i.p. administration of 5 mg/kg metergoline, a non-selective serotonin receptor antagonist. Infusion of 5 micrograms/microliters 8-hydroxy-2-(di-n-propylamino)tetralin, a specific 5-HT1A receptor agonist, into the VTA did not modify the effect of DMI. Besides acting as a 5-HT1B receptor agonist, TFMPP may also act on other 5-HT receptor types, but available evidence suggests that its former action is more important. It thus appears that 5-HT1 receptors in the VTA, presumably of the 5-HT1B type, act by preventing the anti-immobility effect of DMI. The role of VTA dopamine and non-dopamine cells in the effect of TFMPP is discussed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

Decrease in [3H]flunitrazepam receptor binding in rats tolerant to the effects of nitrazepam.

Studies were performed to evaluate the binding of [3H]flunitrazepam to cell membranes from the brain cortex of rats that were made tolerant, by the i.p. administration of nitrazepam once daily, to the anxiolytic and sedative effects (after 14 days) and the anticonvulsant action (electroshock, after 28 days) of nitrazepam. A significant decrease in the number of specific [3H]flunitrazepam binding sites was found only in the group that was tolerant to the anticonvulsant effect. The same experiments were also carried out with oxazepam. Since there were no signs of tolerance, the administration of the drug, 10 mg/kg once daily i.p., was continued for 6 weeks. No tolerance occurred and there were no changes in [3H]flunitrazepam binding site density. We conclude that tolerance to the anticonvulsant effect of nitrazepam could be related to the down-regulation of the benzodiazepine receptors.

Animals↗
PubMed1985

Repeated treatment with amitriptyline reduces immobility in the behavioural 'despair' test in rats by activating dopaminergic and beta-adrenergic mechanisms.

Seven days of treatment with amitriptyline 10 mg kg-1 day-1, reduced the immobility time in the behavioural 'despair' test in rats. 0.5, but not 0.25 mg kg-1 haloperidol significantly counteracted the reduction of immobility caused by amitriptyline. Its anti-immobility effect was reduced by 50 and 100 mg kg-1 sulpiride, another blocker of dopamine receptors, and 5 mg kg-1 (+/-)-propranolol, a beta-adrenolytic drug. Prazosin, 3 mg kg-1, an antagonist of post-synaptic alpha-adrenoceptors, had no effect. It is suggested that dopaminergic and beta-adrenoceptors mediate the anti-immobility effect of repeated amitriptyline treatment in rats.

Amitriptyline↗
PubMed1984

Effect of repeated treatment with desipramine in the behavioral "despair" test in rats: antagonism by "atypical" but not "classical" neuroleptics or antiadrenergic drugs.

A 7-day treatment with 20 mg/kg/day desipramine reduced the immobility time in the behavioral "despair" test in rats. The effect of DMI was antagonized by sulpiride (100 mg/kg i.p.), metoclopramide (20 mg/kg i.p.) and clopazine (20 mg/kg i.p.) but not by haloperidol (0.5 mg/kg i.p.) or chlorpromazine (5 mg/kg i.p.). Alpha-adrenoreceptor blockers (prazosin 3 mg/kg s.c.; aceperone 10 mg/kg i.p.; azapetine 24 mg/kg s.c.; phentolamine 20 mg/kg i.p.), dl-propranolol (5 mg/kg i.p.) and clonidine (0.1 mg/kg i.p.) failed to modify the anti-immobility effect of DMI. The data suggest that a particular subtype of dopamine receptors is involved in the anti-immobility effect of a 7-day treatment with DMI in the behavioral "despair" test in rats.

Adrenergic alpha-Antagonists↗
PubMed1984

Effects of agents increasing serotonin transmission on the increase of dopamine metabolism caused by morphine in the rat nucleus accumbens.

The effect of subcutaneous injection of 10 mg/kg morphine on homovanillic acid (HVA) concentrations in the nucleus accumbens was studied in rats which had received d-fenfluramine, a serotonin releaser, or m-chlorophenylpiperazine, a serotonin agonist, before morphine. 2.5 mg/kg d-fenfluramine or m-chlorophenylpiperazine had no effect on HVA in the nucleus accumbens but significantly reduced the rise in HVA induced by morphine. None of the drugs modified the levels of morphine in the rat brain. The results suggest that agents increasing serotonin transmission inhibit the effect of morphine on dopamine neurons innervating the nucleus accumbens.

Animals↗
PubMed1981

Ranitidine in the treatment of acute upper gastrointestinal haemorrhage--a comparative study. Preliminary report.

50 patients with acute gastrointestinal bleeding (GIB) were randomly allocated to treatment with i.v. Ranitidine 50 mg b.d., or to a standard conservative therapy. When possible i.v. administration was replaced by oral ranitidine 150 mg b.d. for a total of up to 10 days. Three subgroups included gastric ulcer, duodenal ulcer and haemorrhagic gastritis. The criteria were: the need for blood replacement, comparison of the endoscopic appearance before and after therapy, and the final outcome of treatment, including the need for surgery. Ranitidine appeared to be superior to the standard treatment, the advantages being due largely to the gastric ulcer cases.

Acute Disease↗
PubMed1979

The effect of tricyclic antidepressants (TA) on the circulatory system in primary arterial hypertension.

The cardio-vascular reactions after i.m. application of 0.4 mg/kg of TA (imipramine, amitryptyline and nortryptyline) were compared in normotonics and patients suffering from essential hypertonia. It was found, that systolic blood pressure decreased significantly after the drugs only in hypertonic patients, whereas diastolic blood pressure fall was marked more in the normotonic group. In both groups, no apparent changes in heart action were noticed after the drugs. The TA caused a stronger increase of urine excretion of NE, E, VMA and NMN and MN in hypertonics than in normotonics.

Amitriptyline↗