Biomedical subjects
Publications and source records attributed to E Nowakowska.
Water immersion was used as the treatment method in a patient with ascites caused by liver cirrhosis resistant to therapy. Application of water immersion caused only a short improvement; it was probably connected with the shortterm natriuretic effect. The joint effect of a diuretics and of the water immersion was beneficial.
The influence of the opioid receptor antagonist naloxone upon the reduced locomotor activity after administration of nitrazepam (NTZ) and upon the increased locomotion after chronic nitrazepam administration was tested. It was found that a single dose of naloxone counteracted both the reduced locomotion after acute administration of nitrazepam as well as the augmented locomotor activity after chronic application of nitrazepam. It is assumed that opioid mechanisms are involved in the locomotor effects of benzodiazepines.
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.
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.
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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.
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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.
Imipramine in doses of 0.35-0.45 mg/kg body weight usually induces a drop in arterial blood pressure; the drop is statistically significant in patients with essential hypertension. In these patients, a significant increase in excretion of catecholamines in urine was observed when compared with a control group. In both groups no changes in heart action were found.
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The action of some antidepressant drugs on the circulatory system was found to have an anticholinergic component.
Administration of 6-OH-DA into the lateral cerebral ventricle did not prevent development of hypertension or influence the effects of administration of tricyclic antidepressant drugs (TA). Injection os 6-OH-DA intraperitoneally prevented development of hypertension, and TA apparently protected against the consequences of administration of 6-OH-DA.
The tricyclic antidepressant drugs: imipramine, opipramol, amitryptiline and nortryptiline inhibit development of experimental arterial hypertension in rats.
Cerebral concentrations of neurotransmitters: noradrenaline, dopamine, serotonin and GABA were assayed in male Wistar rats receiving either a single dose of pethidine, or a prolonged treatment with the drug (twice daily for 21 days, im), leading to tolerance development. In tolerant rats the GABA content in the cerebral tissue was increased, and the activity of serotonergic system (assessed from the changes in 5-hydroxyindoleacetic acid level and serotonin turnover rate) was augmented.
Under tolerance, evoked by multiple doses of pethidine (PD), the serum and brain tissue content of PD was related to diminished analgesic activity. Even though in tolerant rats no enhancement of PD biotransformation in the liver could be recognized (as followed by the measurement of hepatic esterase and N-demethylase activity), the amounts of both PD and nor-PD excreted in urine were increased under tolerance. The authors conclude that the faster disposition of PD may contribute to the development of tolerance.
Anticonvulsant, sedative and anxiolytic effects of the following benzodiazepines, administered chronically by the intraperitoneal route, were assessed: nitrazepam (NTZ), diazepam (DZ), oxazepam (OXZ), chlordiazepoxide (CDX) and temazepam (TMZ). The action of NTZ in tests for sedative, anticonvulsant and anxiolytic effects rapidly changed upon a repeated daily treatment, which suggests development of tolerance, while no tolerance developed to such effects of OXZ. The stimulating effect of DZ was found not earlier than after 5 weeks of chronic treatment, but no tolerance to the anxiolytic action was observed, and the anticonvulsant action was even potentiated. The stimulating action and tolerance to the anxiolytic effects of CDX and TMZ developed rapidly, but was accompanied with an only slight decrease in the anticonvulsant effect.