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Biomedical subjects

G E Brill'

Publications and source records attributed to G E Brill'.

At least 19 recordsLinked to original sources

Changes in lymph microcirculation during pathological stress.

Stress caused by immobilization and acoustic stimulation produces considerable changes in lymph microcirculation. These changes manifested in dilation of microvessels, enhanced phasic contractile activity and its abnormal pattern, accelerated lymph flow, and recruitment of new lymphangions in drainage functions.

Animals↗

[Nitric oxide in the lymphatic microvessel regulation].

Topical application of sodium nitroprusside on rat mesentery has a marked influence on lymph microvessels function. The drug causes a dilation of majority of lymphangions and decrease of the pacemaker activity of the vessel wall structures and valves. These changes do not lead to lymph stasis, and lymph flow velocity does not reduce. The non-selective inhibitor of NO synthase (N-nitro-L-arginine) intensifies vasomotions of lymph microvessels, modulates phasic contractile activity and increases lymph flow velocity. There is a time dependent dynamic of changes in action of N-nitro-L-arginine. During inhibition of endogenous NO synthesis the responses of lymph microvessels on sodium nitroprusside application are modified: the constriction of majority lymphangions and activation of valve work are observed.

Animals↗

[Functional organization of lymphatic microvessels of the rat mesentery].

Lymph flow as measured with biomicroscopic and speckle-interferometrical techniques was very unstable and its rate did not depend on lymphangion diameter in the rat mesentery. A correlation was found between amount of cells in the lymph flow and other indices of lymphangion functions. All microvessels with phasic contractions and/or working valve were revealed as having a lymph flow. The phasic activity and the valve work correlated with each other. The higher the amplitude and frequency of the phasic activity and the longer the contraction cycle, the higher was the rate of the valve work.

Animals↗

[Sex differences in adrenocortical sensitivity and resistance to cerebrovascular damage in rats under strong stress].

Dynamics of changes in adrenal and plasma corticosterone and the development of cerebrovascular lesions were studied in both male and female rats, exposed to strong stress (combined immobilization and intermittent found sound for 2 hours). Plasma corticosterone levels in stressed females were 460% and 660% of the control values when measured on stress minute 10 and 120. The corresponding values in male rats were 220% and 360%. The stress-induced dilatation of brain vessels and the increases in vascular permeability were less pronounced in females than in males, when studied 0.1 and 24 hours after termination of stress. The number of brain perivascular haemorrhages was markedly reduced in females compared with males. It is supposed that higher resistance to stress-induced cerebrovascular lesions in females may be attributed to higher functional reserves of steroidogenesis.

Acoustic Stimulation↗

[Participation of Ca-dependent systems in thrombocyte aggregation induced by the action of staphylococcal toxin and ADP].

The mechanism of ADP and staphylococcal toxin effect on the platelet aggregation has been studied on the rabbit's platelet-rich plasma. Ca2+-channels blockade of the cell membrane by verapamil resulted in considerable inhibition of aggregation induced by ADP and some weakening of toxin action. Binding of extracellular calcium EDTA inhibited sharply or blocked the aggregation of both inductors. It has been concluded that Ca2+ transport into cell is necessary chain in ADP and staphylococcal toxin effect but under the action of toxin transport Ca2+ into platelet is brought through a verapamil-resistant Ca2+-channels forming in the membrane under the interaction with toxin.

Adenosine Diphosphate↗

[Effect of staphylococcal toxin on the microcirculatory system].

Study of microcirculation in the mesentery of narcotized rats showed that the staphylococcal toxin causes increased migration of leukocytes, aggregation of formed elements, and disturbance of the blood flow in the small venules and arterioles. The toxin stimulates rhythmic contractile activity of the lymphatic microvessels and induces their constriction and even complete obliteration. The lymphoconstrictive effect of the toxin is weakened by verapamil and completely removed by dimethyl sulfoxide.

Animals↗