Microcirculatory disturbances in gastric mucosa during ulcer disease and effects of serotonin on their dynamics.

Experiments on rat model of stress-induced gastric ulcers revealed marked circulatory disturbances in ulcerated gastric mucosa associated with arteriolar spasm and venous congestion and leading to perivascular edema, diapedesis of erythrocytes, and microhemorrhages. These changes were most pronounced on day 1 after ulcer modeling and progressively decreased during healing (day 14-21). On day 3, arterial hyperemia developed against the background of venous congestion, which was probably related to progressive repair. Serotonin adipinate administered after ulcer modeling accelerated the development of arterial hyperemia (day 1) and reduced venous congestion and extravascular changes. Pretreatment with serotonin was even more effective in attenuating venous congestion and extravascular changes.

[Mast cell reaction to total irradiation]. / Reaktsiia tuchnykh kletok na obshchee obluchenie.

A morphofunctional changes of peritoneal and mesenteric mast cell populations in rats from first minutes up to 10 day after irradiation in dose 5.5 Gr were studied. It is shown that the increased mast cell degranulation is of the first reactions of organism on irradiation. Mast cell reaction on irradiation is biphasic; the quick, short first phase is observed approximately during 0.5 h after irradiation, the gradual prolonged second phase reaches its peak about 5-12 h and continues at least during 10 days.

[The mechanisms of the stimulating effect of tissue basophils on the reparative processes in inflammation]. / Mekhanizmy stimuliruiushchego vliianiia tkanevykh bazofilov na reparativnye protsessy pri vospalenii.

Mast cells stimulating effect on reparative processes in inflammation involves histamine, serotonin and heparin. This was shown on the model of E. coli-induced acute infectious peritonitis in rats using antagonists of major biologically active mast cells products (histamine, serotonin and heparin)-dimedrole, cimetidine, ciproheptadine and protamine sulfate. Fibroblast accumulation is associated with histamine, influencing predominantly H1- and H2-receptors as well as with serotonin. Fibroblast proliferative synthetic ability increases through histamine action on H1-receptors and serotonin and heparin influence. Accumulation of monocytes-macrophages and their proliferative synthetic ability stimulation is affected by histamine (through H1-receptors) and serotonin.

[The repopulation and regranulation of tissue basophils at the site of acute inflammation]. / Repopuliatsiia i regranuliatsiia tkanevykh bazofilov na meste ostrogo vospaleniia.

Regularities of rat mast cells (MC) repopulation and regranulation in late reparative stage of inflammation compared to that in conditions approximating to MC natural renewal (after their osmiophilic elimination) and MC restoration after the inflammation caused during their absence were established on the model of E.coli induced acute infectious peritonitis. MC number in peritoneal fluid and mesenterium restores by 90th day in typical development of the inflammation, with peritoneal MC regranulation yielding to that in mesenterium and remaining unfinished by 120th day. MC repopulation in peritoneal fluid and mesenterium forestalls the one observed after the osmotic MC elimination. Inflammation, induced during MC absence retards peritoneal MC regranulation and promotes that of mesenterial ones. MC repopulation and regranulation on the site of inflammation combines their degranulation and high content of free histamine in peritoneal fluid and mesenterium.

[Interleukin-1 production by exudate and bone marrow macrophages in experimental acute infectious peritonitis]. / Produktsiia interleikina-1 makrofagami éksudata i kostnogo mozga pri éksperimental'nom ostrom infektsionnom peritonite.

The model of acute infectious peritonitis in mice has been used to show that inflammation is attended by a marked phasic increase in interleukin-1 (IL-1) production by macrophages of exudate and bone marrow. The increased IL-1 production by macrophages of exudate proceeds earlier than that by macrophages of the bone marrow. This indicates that activation of the bone marrow macrophages may be a result of the effect of OL-1 and other haemopoietic factors released by macrophages on the inflammatory focus.

[The role of the leukocytes in the mast cell reaction in an inflammatory focus]. / Rol' leikotsitov v reaktsii tuchnykh kletok ochaga vospaleniia.

Models of acute infectious and aseptic peritonitis in rats with vinblastine-induced leukopenia have shown the regulatory influence of leukocytes on mast cells consisting in antimicrobic and activating effects. While infectious inflammation is characterized by increased mast cell degranulation both before and after marked leukocyte accumulation in the inflammatory focus and blood. Aseptic inflammation is followed by retardation of mast cell reaction to the significant leukocyte influx into inflammatory focus and blood and increased mast cell degranulation after leukocyte influx.

[The effect of mast cells on the T-lymphocyte mechanisms of hemopoiesis regulation in inflammation]. / Vliianie tuchnykh kletok na T-limfotsitarnye mekhanizmy reguliatsii gempoéza pri vospalenii.

It was shown on the model of acute infections peritonitis in mice that the inflammation induced in the absence of mast cells was characterized by increased T-lymphocyte accumulation and macrophage-activating factor production and, in case of Thy-1,2(+)-lymphocyte elimination from bone marrow cell suspension, by earlier suppression of colony-stimulating and erythropoietic activity production by adhering and non-adhering myelokaryocytes. The results indicate that the modulatory effect of mast cells on haematopoiesis in inflammation is due in many respects to T-lymphocyte inhibition.

[The effect of the mast cells on interleukin-1 production by exudate and bone marrow macrophages in inflammation]. / Vliianie tuchnykh kletok na produktsiiu interleikina-1 makrofagami ékssudata i kostnogo mozga pri vospalenii.

It was shown on the model of acute infectious peritonitis in mice that the inflammation induced in the absence of mast cells was characterized by an earlier interleukin-1 (IL-1) production by bone marrow macrophages and by the lack of relapsed IL-1 production by macrophages of both exudate and bone marrow. This correlated with the previous data of the authors on the earlier haematopoiesis activation but weaker bone marrow hyperplasia expression in inflammation induced in the absence of mast cell. The results testify to essential role of mast cells in regulation of IL-1 production by macrophages of exudate and bone marrow. The previously established modulatory effect of mast cells on haematopoiesis in inflammation may be mediated by their effect on IL-1 production by macrophages of the inflammatory focus and haematopoiesis-induced microenvironment.

[Mechanisms of the modulating effect of mast cells on the leukocytic response in inflammation]. / Mekhanizmy moduliruiushchego vliianiia tuchnykh kletok na leikotsitarnuiu reaktsiiu pri vospalenii.

On the model of acute infectious peritonitis in rats with using the antagonists of the main biologic active products of mast cells it is shown that modulating effect of mast cells on the leucocytic reaction in inflammation is realized with the histamine, serotonin and heparin participation; in this way histamine influences mainly through H2-receptors on neutrophils and H1-receptors on monocytes.

[Role of T-lymphocytes in the mechanisms of hemopoiesis-inducing microenvironment activation in inflammation]. / Rol' T-limfotsitov v mekhanizmakh aktivatsii gemopoézindutsiruiushchego mikrookruzheniia pri vospalenii.

On the model of acute infectious peritonitis in mice, the inflammation was shown to accompany pronounced activation of bone marrow haemopoiesis. The increased number of committed precursor cells of erythro- and granulomonocytopoiesis, morphologically differentiated elements and enhancing colony-stimulating and erythropoietic activities of GIM cells origin were shown as well. Thy 1.2+ cells, migrating to bone marrow, were shown to play an important role in hemopoiesis stimulation inflammation. These stimulate the processes of myeloid precursor proliferation directly (by means of lymphokines) and in cooperation with monocytes-macrophages of GIM.

[Influence of mast cells on the regulatory mechanisms of hemopoietic bone marrow in inflammation]. / Vliianie tuchnykh kletok na kostnomozgovye mekhanizmy reguliatsii gemopoéza pri vospalenii.

Acute infectious peritonitis simulated in mice was used to show that previous osmotic deterioration of the abdominal mast cell population significantly influenced the function of hemopoiesis-inducing microenvironment (HIM). The earlier production of the colony-stimulating and erythropoietic activities by the non-adhesive myelokaryocytes and the decreased production of these activities by the adhesive cells have been established. The results obtained evidence that mast cells modulate HIM mediating their influence on hemopoiesis under natural conditions of inflammation.

[Interactions of mast cells and leukocytes in increased vascular permeability in the focus of inflammation]. / Vzaimodeistvie tuchnykh kletok s leikotsitami v povyshenii pronitsaemosti sosudov ochaga vospaleniia.

On the model of acute infectious peritonitis in rats it is shown that the mast cell depletion affected the inflammatory focus vascular permeability mainly in the immediate phase of its increase. Leukopenia inhibited the permeability both in the immediate and delayed phases. The combined depletion of mast cells and leukocytes not only inhibited the degree of vascular permeability increase but strongly affected its kinetics during exudative phase of peritonitis. The results indicate that in the natural conditions of inflammation the mast cell-leukocyte interaction in the vascular permeability increase takes place.

[Role of mast cells in reactions of the blood system in inflammation]. / Rol' tuchnykh kletok v reaktsiiakh sistemy krovi pri vospalenii.

On the model of the acute infectious peritonitis in mice it is shown that the previously osmotic disruption of the peritoneal mast cell population remarkably affects the inflammatory focus, blood and bone-marrow leukocytic reactions. The initial neutrophil accumulation increase and the earlier and more intensive leukocytosis and activation of granulo-monocytopoiesis are established. At the same time the kinetics of monocytes in inflammatory focus is expressed weaker and testifies to the prolongation of the inflammatory response. Thus, in the natural inflammatory conditions mast cells of the inflammatory focus directly or indirectly modulate leukocytes and hematopoiesis.