Role of alimentary hyperglycemia in the pathogenesis of some disturbances of lipid metabolism

Alimentary hyperglycemia in rabbits is accompanied by elevation of the serum cholesterol and triglyceride level and also by a progressive rise in the serum concentration of pre--lipoproteins, carriers of endogenous triglycerides. Feeding hyperglycemic animals with cholesterol for a short time leads to earlier and more marked atherogenic changes in the body than similar feeding of normoglycemic animals.Laboratory of Pathological Physiology, Institute of Experimental Endocrinology and Hormone Chemistry, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Yudaev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 3, pp. 281–283, March, 1976.     

Role of activation of lipid peroxidation in pathogenesis of experimental plague intoxication

Activation of lipid peroxidation, increasing during the elevation of clinical symptoms of Y. pestis intoxication and hypoxic syndrome development, is the efferent link in cytopathogenic effects of toxic and enzymatic factors of this microorganism. Absolute or relative insufficiency of enzymatic mechanisms of blood antioxidant protection systems is the main pathogenic factor in lipid components of biomembrane destruction leading to the haemorrhagic syndrome development in Y. pestis intoxication.     

Features of blood lipid composition during emotional stress in rabbits with dyslipoproteinemia

Only the concentration of essential fatty acids increases in blood serum under the effect of emotional stress in intact rabbits. In experimental dyslipoproteinemia, emotional stress, besides increasing the amount of essential fatty acids also causes marked changes of lipid metabolism of an atherogenic character. The mechanisms of lipidemia activation and maintenance are discussed.     

Treatment of dyslipoproteinemia by systemic enzyme therapy in experimental glomerulonephritis

Patients with chronic glomerulonephritis (CG) develop disturbances of lipid blood spectrum leading to additional damage to renal structure. The existent methods of pathogenetic therapy have no effect on lipid imbalance. Recently, many autoimmune diseases have been treated with systemic enzyme therapy (SET). The authors studied SET effect in disturbed lipid metabolism in experimental glomerulonephritis. Experimental animals showed morphological and biochemical changes similar to those in CG of man. SET reduced renal tissue damage and symptoms of dyslipoproteinemia.     

Role of dyslipoproteinemia in the genesis of chronic hepatitis

Laboratory of Experimental Pathomorphology, Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow. (Presented by Academician of the Russian Academy of Medical Sciences D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 10, pp. 437–439, October, 1992.     

Role of intestinal hormones in the pathogenesis of experimental pancreatitis

The course of disturbances of secretory reactions of the pancreas in response to adequate stimulation by intestinal hormones was studied in acute experiments on dogs with preinduced pancreatitis. Activity of combined preparations of intestinal hormones obtained from the duodenal mucosa was found in the acute period of the disease in these dogs. In chronic experiments an increased rate of acid formation in the stomach and a change in the pH of the duodenal contents toward the acid side in pancreatitis were found in chronic experiments. It is concluded that intestinal hormones play an important pathogenetic role in the mechanism of disturbances of the external secretory activity of the pancreas in pancreatitis.Laboratory of Pathophysiology of Digestion, Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. M. Chernukh.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 9, pp. 289–292, September, 1978.     

Role of neutrophils in the pathogenesis of experimental vasculitis.

In the Brown-Norway rat, mercuric chloride (HgCl2) induces an autoimmune syndrome characterized by high IgE levels. There is widespread necrotizing leukocytoclastic vasculitis involving lung, skin, mucous membranes, pancreas, liver, and gut, with tissue injury being most marked in the cecum. As in systemic vasculitis in man, there are neutrophils at the site of tissue injury and the animals develop anti-neutrophil cytoplasmic antibodies, which in the Brown-Norway rat are directed against myeloperoxidase. To determine whether neutrophils are involved in the pathogenesis of the vasculitis, we have used a monoclonal antibody that was reported to deplete neutrophils in other rat strains. Rats treated with HgCl2 received antibody by intravenous injection at various time points. Serial blood samples were taken for neutrophil counts and to assay for anti-myeloperoxidase and IgE antibodies. The guts of animals killed after antibody therapy were scored for vasculitic changes and neutrophils infiltrate. RP3 (but not the control antibody MAC6) was shown to bind to Brown-Norway rat neutrophils and to block glycogen-induced influx of neutrophils into the peritoneum. When given at peak disease, RP3 caused a dose-dependent reduction in tissue injury with a marked reduction in circulating blood neutrophil numbers and in tissue neutrophil infiltrate. RP3 treatment did not affect the rise in titer of IgE and anti-myeloperoxidase antibodies. The data presented demonstrate that in this model neutrophils are necessary for the induction of vasculitis and that the degree of vasculitis correlates with neutrophil number. To our knowledge, this study is the first to provide direct evidence for a role for neutrophils in vasculitis. We suggest that antibodies directed against neutrophils, especially if they deplete neutrophils, may be useful in the therapy of vasculitis in man.     

Effect of amiridin and piracetam on memory disturbances induced by experimental stress

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 115, N ^o 2, pp. 155–157, February, 1993.     

Effect of an antioxidant of the 3-hydroxypyridine class on microcirculatory disturbances associated with experimental dyslipoproteinemia and its alimentary correction

Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR. Research Institute of Pharmacology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 109, No. 3, pp. 234–237, March, 1990.     

Role of T lymphocytes in the pathogenesis of experimental autoimmune encephalomyelitis

A dichotomy between clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) was demonstrated in neonatally thymectomized (NNTx) rats. Although neonatal thymectomy prevented subsequent induction of clinical EAE in Lewis rats challenged as young adults with syngeneic basic protein (BP) of myelin, there was a 50 % incidence of histological EAE. Both cellular and humoral immune responses to BP were reduced in the NNTx rats. However, the presence of a cell-mediated response to BP (MIF release) was statistically associated with the occurrence of histological EAE. Diminished preimmunization blood lymphocyte counts and impairment of the response of spleen cells to phytohemagglutinin were associated with reduced antibody responses. This suggests that collaboration between T and B cells may be necessary for production of antibody to BP. The relationship between antibody and clinical EAE is not clear and warrants further investigation.