[Biochemical mechanisms of the effect of prostaglandin E2 on the effect of parenteral nitrogenous nutrition]. / Nekotorye biokhimicheskie mekhanizmy vliiania prostaglandina E2 na éffekty parenteral'nogo azotistogo pitaniia.

Activation of lipid peroxidation (LPP) processes in the hepatocytes of animals suffering from toxic hepatitis leads to disorders of membrane function and causes disorders of transports processes (activity of adenosine triphosphatase, active sodium transport) in them. Administration of prostaglandin E2 (PGE2) as a potent antioxidant simultaneously with casein hydrolysate to animals with experimental pathology intensifies the effect of the nitrous preparation and promotes normalization of the studied processes (LPP, adenosine triphosphatase activity, active sodium transport). Thus, through its action on LPP and the transport systems, PGE2 influences the effect of casein hydrolysate.

[The effect of prostaglandin E2 on transport processes in the hepatocytes during parenteral feeding against a background of protein starvation]. / Vliianie prostaglandina E2 na transportnye protsessy v gepatotsitakh pri parenteral'nom pitanii na fone belkovogo golodaniia.

Experiments were conducted in 50 white rats (180-220 g bw). Activities of total, Mg2-dependent, Na+, K+ and Ca2(+)-ATPases and sodium transport in hepatocytes of the animals under normal conditions and in the presence of protein deficiency were studied in five test series. Protein deficiency was found to be attended by a significant rise in the activity of the enzymes studied, and by disorders in sodium transport in hepatocytes. Administration of casein hydrolysate, in the presence of protein deficiency in the animals, induced a tendency to normalization of the processes studied. Casein hydrolysate used simultaneously with PGE2 produced more pronounced changes in ATP activity and sodium transport in hepatocytes. Basing on the results of the investigations it has been suggested that casein hydrolysate effect can be intensified by PGE2, thus it can be widely used in clinical practice.

[Effect of prostaglandin E2 on enzyme activity during parenteral feeding]. / Vliianie porstaglandina E2 na aktivnost' nekotorykh fermentov pri parenteral'nom pitanii.

It has been shown that prostaglandin E2 increases the activity of aspartate aminotransferase, alanine aminotransferase in the liver and striated muscle in parenteral feeding and increases the activity of aldolase in the liver but reduces it in the striated muscle. This demonstrates the enzymatic component in the mechanism of action of prostaglandin E2 on organ-tissue metabolism in parenteral feeding.

[A chronic hyperimmunocomplex process and its interrelationship with free radical-generating systems]. / Khronichnyi hiperimunokompleksnyi protses ta ioho vzaiemozv'iazok z systemamy, shchi heneruiut' vil'ni radykaly.

On chronic hyperimmunocomplex process (CHIP) model in rats of Wistar line (Cochrane C., Koffen D., 1973) we determined cAMP and cGMP concentration, nitrogen oxide (NO), urine, urine acid,--in muscle and clearance organs, and also in plasma. In result of carried out investigations there was determined the increase of large and middle CIC in blood plasma, their fixation on endothelium of aorta bifurcation and glomerula basal membrane, partially on liver cells. There was revealed considerable disbalance of cyclic nucleotides concentration in kidneys homogenates, spleen and plasma, with guanils fall (adenil index, what is interconnected with NO level lowering in all cases and urine increase in plasma, simultaneously with its decrease in number--in kidneys and spleen. Urinic acid increased in number in kidneys, spleen, plasma. These changes create favourable background for damaging of endothelium-neutrophil-thrombocyte cooperation through hemokinin, moleculo-adhesive, fermentative mechanism with further development of proliferative-remodulating processes in vessel wall.

[The participation of neutrophilic mechanisms in the pathogenesis of chronic elevated blood immune complexes]. / Uchast' neitrofil'nykh mekhanizmiv u patohenezi khronichnoï hiperimunokompleksemiï.

For reproduction of chronic hyperimmunocomplexemia model the classic Cochrane C. G., 1973 elaboration was used. The circulating immune complexes (CIC) were identified by precipitation methods, and fixated--by immunofluorescent in endothelium reproduction of aorta, and their clearance organs--liver and spleen. The estimation of neutrophil status was carried out according to rosette-forming neutrophils ability--by latex, zimosane, mieloperoxidasa, NST tests. The growth of large and middle CIC in vessel bed was estimated, their fixation in aorta bifurcation, and also on liver and spleen calls, but their intensivity is less, comparing to aorta endothelium. The neutrophil status was characterised by O-neutrophils growth, strengthening of capturing macrophages function, considerable activation of fermentative polynuclear systems, although reserve possibilities in them grew in less degree. Morphologic investigations allow to speak mediatingly about neutrophils participation in endotheliocytes damage, and also about their ability to secure the mononuclear cells further participation in damaging of aorta walls and partially of liver and spleen.