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Yakovlev, M. Yu.

doi:10.1023/a:1024989709554

Cited by 11 publications

(4 citation statements)

References 7 publications

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“…Stress also induces endotoxaemia in tissue injuries primarily by increasing the intestinal barrier (de Punder and Pruimboom 2015). Bacterial toxins (LPS) that enter the bloodstream, in turn, stimulate neutrophilia (Yakovlev 2003).…”

Section: Changes In Granulocyte Numbermentioning

confidence: 99%

Effects of 1,3,4-thiadiazine compound with antidepressant properties in ligation model of acute pancreatitis

Sarapultsev¹,

Чупахин²,

Rantsev³

et al. 2018

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Based on hypotheses concerning the role of stress in acute pancreatitis development, the experimental approach for the decrease stress damage via the use the compound with proven antistress/neuroleptic action was conducted. The study was aimed to discover 2-morpholino-5-phenyl-6H-1,3,4-thiadiazine hydrobromide (compound L-17) therapeutic action in experimental acute pancreatitis. The experimental model used was the ligation model. The trial was carried out on 50 male Wistar rats with average body weight 180-240 g. Histological picture of the pancreas was studied and biochemical and enzyme-immunoassays were carried out on the first and seventh days. The significant reduction in mortality on the background of L-17 compound administration was observed. While levels of all cytokines increased in induced experimental acute pancreatitis groups, the cytokine level rise was decreased when compound L-17 was administered. On the cellular level, the study revealed L-17's ability to prevent granulocytosis and decrease granulocytes infiltration to inflammatory foci. The decrease in inflammatory reaction magnitude and prevention of abscess formation in experimental acute pancreatitis accompanied by sistemic inflamamtion was due to L-17's ability to reduce neutrophilia and neutrophil entry into the injury zone.

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Section: Changes In Granulocyte Numbermentioning

confidence: 99%

Effects of 1,3,4-thiadiazine compound with antidepressant properties in ligation model of acute pancreatitis

Sarapultsev¹,

Чупахин²,

Rantsev³

et al. 2018

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“…According to the present views [27][28][29][30][31][32], the intestinal endotoxin (ET), which is formed when the gram-negative intestinal microflora, mainly Escherichia coli, is killed, acts as the leading agent initiating activation of SN and the entire granulocytic system and defining the similarity between the mechanisms of adaptation and pathology in case of inflammation [33][34][35][36]. This is a natural metabolite, a lipopolysaccharide (LPS) by its chemical nature.…”

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confidence: 99%

“…LPS is constantly present in the systemic blood of healthy people and animals, and can be detected in the blood serum and SN in very low concentrations. This phenomenon was named the systemic endotoxinemia (SEI) [29,30]. About 95 % of ET synthesized in the intestine is bound by resident macrophages of the liver and also excreted through kidneys, mucous membranes and skin [42].…”

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confidence: 99%

“…In case of failure of LPS-eliminating systems, its concentration in blood may increase several times, which is defined as the en-dotoxin aggression (EA) [49][50][51]. If the systemic endotoxinemia represents an adaptive physiological phenomenon [27,30], the endotoxin aggression is a general pathological phenomenon since, according to the endotoxin theory [30,52], it is a universal agent in the development mechanisms of the majority of principal infectious [53,54] and non-infectious diseases [55,56], and symptom complexes. The transformation of SEI into EA undergoes all stages (from the compensation and stress to subcompensation and decompensation) typical for the development of other forms of endogenous intoxication.…”

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confidence: 99%

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ENDOGENOUS INTOXICATION AND INFLAMMATION: REACTION SEQUENCE AND INFORMATIVITY OF THE MARKERS (review)

Sidel'nikova¹,

Chernitskiy²,

Retsky³

2015

S-h. biol.

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According to modern phylogenetic theory of general pathology (V.N. Titov, 2003, 2013) inflammation is a nonspecific biological reaction, providing the removal of excessive amount of highmolecular macromolecules and maintenance of metabolic homeostasis (endoecology). The increase of any metabolite concentration above the physiological range is a violation of the «purity» of intercellular medium. This triggers two nonspecific biological reactions, namely the excretion used to remove «biological waste» of a molecular weight less than 70 kD and the inflammation in case the larger molecules and their complexes should be removed via neutrophils, resident macrophages and endothelial cells. Blood concentration of leukocytes has been used for evaluation of inflammation and intoxication activity for many decades. However, at the molecular level there is a requirement in precise differentiation of metabolites, activating leukocytes, and metabolites, excessively forming as a result of activation, because the last disturb molecular homeostasis and may damage cells and tissues. Validity of leucocytal intoxication index (LII) of Ya.Ya. Kalf-Kalif, concentration ratio of low and medium molecular weight substances, average molecular peptides, total and effective albumin as markers of endogenous intoxication (M.Ya. Malakhova, 2005) are considered. It is shown that primary agent, activating neutrophils and some factors of humoral immunity, is a lipopolysaccharide (endotoxin) of gram-negative microflora (M.Yu. Yakovlev, 2003; O.W. McIntyre, 2011). An excess of endotoxin inflow is possible under intestine and liver pathologies, and due to sympathoadrenal system activation, and also with feed and air. The overload of systems and organs of elimination of endotoxin causes secondary immunodeficiency, which becomes the cause of acute and chronic inflammatory processes of various localizations. It is offered to consider lipopolysaccharide of gramnegative microflora as a primary agent of endogenous intoxication and all the metabolites, produces at increased concentrations as a result of polymorphonuclear leukocytes activation such as reactive oxygen species, oxidated proteins, products of lipid peroxidation and proteolysis, as a secondary one. Such an approach allows to single out various points of application for therapy of endogenous intoxication: i) elimination of excessive concentration of lipopolysaccharide in blood by limiting its production and income from internal and external sources, as well as by a variety of methods of active binding and excretion of endotoxin (S.V. Smirnov et al., 2003; K. Battenschoen et al., 2010); ii) reducing the concentration of «secondary» metabolites in blood and tissues.

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Increased titers of antibodies to bifidobacteria as a marker of intestinal dysbacteriosis

et al. 2005

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Cited by 11 publications

References 7 publications

Effects of 1,3,4-thiadiazine compound with antidepressant properties in ligation model of acute pancreatitis

Effects of 1,3,4-thiadiazine compound with antidepressant properties in ligation model of acute pancreatitis

ENDOGENOUS INTOXICATION AND INFLAMMATION: REACTION SEQUENCE AND INFORMATIVITY OF THE MARKERS (review)

Increased titers of antibodies to bifidobacteria as a marker of intestinal dysbacteriosis

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