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Biomedical subjects

J Moniuszko-Jakoniuk

Publications and source records attributed to J Moniuszko-Jakoniuk.

At least 19 recordsLinked to original sources
PubMed1990

The influence of lead ions on uterine activity in the rat.

Spontaneous uterine activity and reactivity to oxytocin, naproxen and PGF2 alpha were studied in vitro in 80 rats, which for 2-8 weeks had been exposed to different concentrations and combinations of Pb2+, Zn2+ and Cu2+ in their water supply or had been given clean water for control. In rats given only Pb2+ in concentrations of 1000 and 500 ppm for 6 weeks the uterine activity was significantly increased, whereas in groups given the other ions alone, or Pb2+ for 6 weeks followed by 2 weeks of clean water or Zn2+ or Cu2+ no change was observed. The responses to the oxytocin, naproxen and PGF2 alpha did not differ. These results suggest that contamination with lead ions might be one of the etiological factors involved in conditions with increased uterine activity.

Animals↗
PubMed1988

[Evaluation of iron metabolism in workers exposed to led compounds in a tile glaze factory 1981-1982].

The investigations have been aimed at an estimation of the iron balance in lead-exposed workers. The investigations were carried out in a group of 20 men producing lead glazes and a control group of 23 Medical Academy students. Lead concentration was found to be remarkably higher in the exposed group, as compared to the controls. In the control group 26% of subjects exhibited lead concentration within 40.5 micrograms/dm3. The obtained results of D-aminolevulinic acid concentrations in the exposed patients' urine did not differ from the controls. Toxic effects of lead on haem synthesis resulted in significantly higher concentration of iron and transferin saturation percent as compared to controls. The excessive concentration of lead found in the urine of 26% of students points to non-professional exposure.

Adult↗
PubMed1983

Examinations on contribution of bradykinin in the action of dopamine in circulatory system of rats. II. Influence of bradykinin in the action of dopamine on the vessel perfusion of the isolated hindpaw of rats.

The influence of different doses of bradykinin (0.1 micrograms, 1.0 micrograms/0.1 ml) and dopamine (0.1, 0.25, 0.5 micrograms/0.1 ml) on the flow through vessels of the isolated hindpaw of rat was estimated. Dopamine in small doses did not change and in the highest doses decreased the vascular flow. Bradykinin decreased the vascular flow and the effect was dose-dependent. This peptide administered together with dopamine in the smallest dose, evoked the same effect as dopamine itself in the highest dose and decreased the effect of dopamine introduced into the organism in the highest dose. Administration of phentolamine and propranolol decreased the vascular flow. The vasodilating effect of dopamine was seen after administration of drugs blocking the adrenergic receptors and the vaso-constricting effect of dopamine administered in the highest dose was not observed. Bradykinin decreased the vascular flow and when administered together with dopamine evoked effect similar to that after administration of the peptide with phentolamine and propranolol. The authors suppose that except the modifying influence of bradykinin on the action of dopamine, the role of the peptide receptor in this action cannot be excluded.

Animals↗
PubMed1983

Examinations on contribution of bradykinin in the action of dopamine in circulatory system of rats. I. Influence of bradykinin in the action of dopamine on arterial blood pressure of rats.

The influence of different doses of bradykinin (2.5 micrograms, 5 micrograms/kg i.v.) and dopamine (0.5 micrograms - a small dose and 25 micrograms, 250 micrograms/kg i.v. - a big dose) administered into the rat femoral artery on the blood pressure was estimated. Dopamine evoked hypotension (the small dose) or hypertension (the big dose). Bradykinin evoked dose-dependent decrease of the blood pressure. Bradykinin (2.5 micrograms/kg i.v.) administered in the 45th sec of the dopamine action enhanced the hypertensive effect and decreased the hypotensive effect of dopamine. Dopamine administered in the big dose after phentolamine and propranolol evoked hypotension. This effect was stronger after administration of dopamine (25 micrograms/kg i.v.). The hypotensive action of bradykinin persisted in spite of phentolamine and propranolol application but this peptide did not change the hypotensive effect of dopamine under these conditions. The authors discuss hypothetical mechanism of action of the observed influence of bradykinin on the effect of dopamine in the circulatory system.

Animals↗
PubMed1983

Examinations of contribution of bradykinin in the action of dopamine in circulatory system of rats. III. Influence of bradykinin on chosen metabolic effects of dopamine.

The influence of bradykinin on the action of dopamine in the biochemical examinations (the activity of phosphorylase "a" in the heart muscle, the level of free fatty acids and the level of lactic acid in blood) were estimated. It was shown that dopamine (250 micrograms, 500 micrograms, 750 micrograms/kg i.v.) increased and bradykinin (2.5 micrograms, 5 micrograms/kg i.v.) did not change the examined biochemical parameters. Bradykinin applied in the smaller dose simultaneously with dopamine in the smallest dose intensified the amine action. The peptide introduced into the organism in the higher dose increased the stimulatory action of dopamine as estimated by the of phosphorylase "a" activity in the heart muscle and diminished the amine effect as estimated by the free fatty acids and lactic acid in blood. Administration of bradykinin with dopamine in the highest dose - 500 micrograms/kg i.v., did not change the stimulatory action of the catecholamine. But application of bradykinin with dopamine in the highest dose diminished the stimulatory effect of the dopamine. Therefore, bradykinin modified the action of dopamine as it was demonstrated by the estimation of the metabolic effects.

Animals↗
PubMed1980

Biological effects of degradation products of collagen by bacterial collagenase.

1 Collagen degradation products (CDP) resulting from bacterial collagenase digestion were fractionated by gel filtration and their biological activities in rats were estimated. 2 CDP induced the following kinin-like effects: increase in permeability of skin blood vessels, contraction of the isolated intestine of the rat, depression of locomotor activity and of motor coordination. 3 The most active CDP fraction was CDP III containing peptides of mol. wt. < 1000 D with a high percentage of hydroxyproline. 4 As compared with bradykinin, CDP III was less active in the skin permeability test and was 15,000 to 20,000 fold less effective in induction of isolated intestine contraction. 5 Depression of the CNS induced by 30 microgram of CDP III administered into the brain ventricle was similar to that observed after 4 microgram of bradykinin given by the same route. 6 CDP III prolonged the duration of sleep evoked by thiopentone and enhanced the threshold of convulsion induced by pentazol. 7 The activity of CDP in comparison to other low molecular weight peptides is discussed.

Animals↗
PubMed1976

Investigations of the mechanism of central action of kinins.

The effects of kinins on the level of norepinephrine, dopamine, and serotonin and on their metabolites, i.e., normetanephrine, homovanillic acid, and 5-hydroxyindoloacetic acid in the brain tissue divided into cerebellum, corpus striatum, cortex, hippocampus, hypothalamus, medulla oblongata, and midbrain were investigated. It was shown that bradykinin in a dose of 4 mug decreased the content of norepinephrine in corpus striatum, midbrain, and cerebellum. It also decreased the level of dopamine in corpus striatum but increased the level of serotonin in corpus striatum and midbrain. Similar changes were observed with 100 Mu/kg of kallikrein. It was that changed levels of investigated neuromediators are accompanied by changed levels of their metabolites. Bradykinin, in a dose of 4 mug, decreased the level of normetanephrine in corpus striatum, hippocampus, and midbrain and the level of homovanillic acid in corpus striatum, and increased the level of 5-hydroxyindoloacetic acid in corpus striatum and hippocampus. It was also shown that bradykinin increased norepinephrine uptake by the blood platelets when its level in the platelets was low, and released the absorbed norepinephrine into the medium when the level of norepinephrine was higher. The above results confirm the existence of an interaction of kinins with neuromediators in the central nervous system.

Animals↗