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Biomedical subjects

G V Poriadin

Publications and source records attributed to G V Poriadin.

At least 19 recordsLinked to original sources

[Immunologic disorders in pathogenesis of chronic generalized parodontitis].

Systemic immunity was studied in patients with chronic generalized parodontitis. This group of patients had distinct changes in immunologic system: depression of T- and stimulation of B-cellular immunity without accumulation of plasma cells and initiation of effective humoral response. Increased peripheral blood number of lymphocytes expressing induction of apoptosis CD95 receptors and ligand for this receptor CD95L (Fas-L) can lead to intensification of lymphocyte apoptosis and may be the reason for T-cell deficit development. The results of the study confirm the important role of immune system disturbances in pathogenesis of chronic generalized parodontitis.

Apoptosis↗

[The restitution of the population of the mesenteric mast cells of the rat intestine].

Reparative processes in rat mesentery mast cells after their depletion by injection of distilled water were studied. In accordance with mast cell localization common population was divided into two subpopulations: paravascular and membranous located in a zone free from blood vessels. Only membranous subpopulation localized in "mesenteric windows" was destroyed by hypo-osmia. At the same time paravascular mast cells were not destroyed. Destructive processes in membranous zones were associated with an increase in the number of paravascular mast cells. Subsequent gradual colonization of mesenteric areas destroyed by distilled water resulted in decrease in the number of mast cell associations along blood vessels. A similar inversely proportional relationship between mast cell count in vessel-free zones and number of mast cell associations near blood vessels was observed in intact mesentery as well. We suppose that the processes of violent destruction of rat mesentery mast cells as well as their natural death stimulate a compensatory increase of their counts in paravascular zones.

Animals↗

[Suppressor activity changes in human T-lymphocytes as affected by adreno- and cholinotropic substances].

The influence of oxyfedrine (beta-adrenoagonist) and carbocholine (cholinoagonist) on the functional activity of Con A-induced suppressor T-lymphocytes in healthy persons and in bronchial asthma patients was studied. Oxyfedrine at a concentration of 10 micrograms/ml (10(-5) M) was shown to induce a significant increase in the suppressing activity of both normal lymphocytes and those obtained from bronchial asthma patients. The repeated incubation of lymphocytes with carbocholine at a concentration of 5 micrograms/ml (10(-6) M) led to the removal of the suppressing effect of normal lymphocytes and to the increase of the activating effect of lymphocytes from bronchiae asthma patients.

Asthma↗

[Suppressant effect of oxyfedrine on development of anaphylaxis in experimental animals].

Oxyfedrine (ildamen) which stimulates beta-adrenoreceptors of smooth muscles in concentrations increasing the tissue content of cAMP produced a dose-dependent inhibition of anaphylactic bronchospasm and contractions of the guinea-pig intestine induced by administration of ovalbumin. The results obtained provide evidence in favour of oxyfedrine use for suppression of immediate type allergic reactions with the involvement of smooth muscles.

Anaphylaxis↗

[Reproduction of the anaphylactic reaction of isolated human smooth muscle organs and the effect of several adrenotropic substances].

A comparative study was carried out of passive sensitization of the lungs, bronchi, small and large intestine by the blood sera of patients sensitive to ambrosia pollen. Passive sensitization and subsequent anaphylactic contraction were reproduced on the isolated bronchi, lungs and the ileum. Development of this reaction was less constant in the large intestine, jejunum and the appendix. The value of anaphylactic reaction of human smooth muscle displayed significant changes with the treatment of the muscles by agents selectively acting on the beta-adrenergic receptors of these organs.

Anaphylaxis↗