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B Malinowska

Publications and source records attributed to B Malinowska.

71 records · Page 4Linked to original sources
PubMedDate not supplied

Attenuation of the acute amnestic effect of ethanol by ifenprodil: comparison with ondansetron and dizocilpine.

The aim of the present study was to examine the influence of ifenprodil, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist which also blocks 5-HT3 receptors, on the amnestic effect of ethanol in a passive avoidance task in mice. The anti-amnestic action of ifenprodil was compared with the effects of the 5-HT3 receptor antagonist ondansetron and the non-competitive NMDA-receptor antagonist dizocilpine (MK-801). Ethanol, 2 g/kg and dizocilpine 0.1 mg/kg significantly impaired the passive avoidance response. In contrast, ifenprodil (0.1-10 mg/kg), ondansetron (0.03-0.3 mg/kg) and dizocilpine (0.01 and 0.03 mg/kg) did not alter passive avoidance by themselves. Dizocilpine did not diminish the amnestic action of ethanol when administered at doses of 0.03-0.1 mg/kg. However, the amnestic effect of ethanol was partially restored towards normal by ifenprodil 0.3 mg/kg and by ondansetron 0.03 mg/kg (alone or together with dizocilpine 0.01 mg/kg) but it was not affected by other doses of ifenprodil (0.1, 1 and 10 mg/kg) and ondansetron (0.1 and 0.3 mg/kg). In conclusion, ifenprodil at an appropriate dose reduced ethanol-induced amnesia in a step-through passive avoidance task. The results are compatible with the assumption that the anti-amnestic action of ifenprodil may be (at least partially) due to an antagonism at 5-HT3 receptors.

Acute Disease↗
PubMedDate not supplied

Three new derivatives of 3-amino-1,2-propanediol; their spectral properties and biological evaluation.

Three new derivatives of 3-amino-1,2-propanediol have been synthesized. Full assignments of signals in their 1H- and 13C-NMR spectra are given. The influence of these compounds on the cardiovascular system in the anaesthetized rat was examined. In contrast to CGP 12177 which induced a strong increase in heart rate and a slight increase in blood pressure, compounds 1, 2 and 3 x HCl at doses up to 1 micromol/kg and compound 3 at doses of 0.01 and 0.1 micromol/kg did not change the cardiovascular parameters. The highest dose of compound 3-1 micromol/kg caused a very short-lasting decrease in heart rate (by 14%) and in blood pressure (by 25%).

Animals↗
PubMedDate not supplied

The effect of ethanol and serotonin on blood vessels of the rat.

In in vitro conditions ethanol dose-dependently contracts the isolated tail artery and aorta of the rat. In concentration 0.03 M ethanol did not change the perfusing pressure in isolated vessels, but potentiated the contracting action of serotonin. In concentration of 0.1 M ethanol did not change the sensitivity of blood vessels to serotonin, and in concentration of 0.3 M inhibited it. Statistically significant changes were observed only in tail artery. The tail artery isolated from the rat receiving a single dose of ethanol (2 g/kg) displayed decreased sensitivity to action of serotonin. Chronic administration of ethanol (6 g/kg/day for 14 days) did not change the serotonin-induced contraction of the isolated tail artery of the rat. The present data indicate that ethanol modifies the sensitivity of rat blood vessels to serotonin.

Animals↗
PubMedDate not supplied

The influence of propranolol on the hypotensive action of ketanserin in normotensive rats.

In normotensive rats the effect of different doses of propranolol (1.0, 5.0 and 10.0 mg/kg i.p.) and ketanserin (10.0 mg/kg p.o.) on mean blood pressure and heart rate and on cardiovascular response to noradrenaline (0.1, 0.3, 0.5, 0.7 and 1.0 micrograms/kg i.v.) was examined. The drugs were given separately or together. Propranolol slightly reduced the hypotensive effect of ketanserin. On the other hand a decrease in heart rate caused by propranolol was not affected by ketanserin. Our results show that propranolol given with ketanserin did not change the effect of the latter on the cardiovascular system.

Animals↗
PubMedDate not supplied

The effect of verapamil on serotonergic mechanisms in the rat blood platelets.

Verapamil in vitro inhibits the uptake and enhances the release of the labeled serotonin from the rat blood platelets. It also inhibits the facilitating action of serotonin on the aggregation response of platelets stimulated by ADP. The obtained results indicate that verapamil significantly influences serotonergic mechanisms in the blood platelets, at least in the rat.

Animals↗
PubMedDate not supplied

The effect of ethanol on some serotonergic mechanisms in rat blood platelets.

Under in vitro conditions ethanol inhibits the uptake and enhances release of [14C]-5HT from rat blood platelets. Similar results were obtained in blood platelets isolated from the blood rats receiving 2 g/kg ethanol. Ethanol decreased also the 5-HT content in the blood platelets. It inhibited the aggregation of blood platelets but did not change the potentiating action of 5-HT on ADP-induced aggregation. The results indicate that ethanol by its action on the transport mechanisms in blood platelets may elevate the level of free 5-HT in the blood plasma, in this manner potentiating the action of the amine in the circulatory system.

Adenosine Diphosphate↗
PubMedDate not supplied

Lack of the specific influence of histamine and histamine H1, H2 and H3 receptor ligands on the serotonin uptake and release in rat blood platelets.

This work was designed to investigate the influence of histamine, and H1 receptor agonist 2-(2-thiazolyl)ethylamine, H2 receptor agonist dimaprit and H3 receptor agonist R-(-)-alpha-methylhistamine on the serotonin uptake and release in rat blood platelets. Histamine and R-(-)-alpha-methylhistamine (up to 1 mmol/l), 2-(2-thiazolyl)ethylamine (up to 10 mumol/l) and dimaprit (up to 1 mumol/l) failed to affect the serotonin uptake. The concentration-dependent inhibitory effects of higher concentrations of 2-(2-thiazolyl)ethylamine and dimaprit (up to 1 mmol/l) were not diminished by the H1 receptor antagonist dimetindene and the H2 receptor antagonist ranitidine (1 and 100 mumol/l each), respectively. Histamine, 2-(2-thiazolyl)ethylamine, dimaprit and R-(-)-alpha-methylhistamine (up to 10 mumol/l) did not change the serotonin release from rat blood platelets. Our results demonstrate that histamine and histamine H1, H2 and H3 receptor agonists do not affect in a specific manner the serotonin uptake and release in rat blood platelets.

Animals↗