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Biomedical subjects

A M Ul'ianov

Publications and source records attributed to A M Ul'ianov.

At least 19 recordsLinked to original sources
PubMed1987

[Decreased sensitivity to the hypoglycemic action of insulin in animals with a lowered blood heparin concentration].

It has been shown that in animals with reduced heparin blood concentration the hypoglycemic insulin action was considerably low. This was established for rats with alloxan diabetes and ageing rats with depressed anticoagulation system and atherosclerosis enhanced by prolonged atherogenic diet. With insulin injection (0.2-0.3 U/200 g), blood sugar concentration in such animals was 2-2.5 times lower than in normal ones. The compensation of endogenous heparin deficiency by an intravenous injection of heparin normalizes the reaction of animals to exogenous insulin.

Animals↗
PubMed1986

[Dependence of the blood plasma activity of the diabetogenic factor in animals on the functional depression of the anticoagulating system induced by an atherogenic diet].

It has been found that in blood plasma of rats keeping on an atherogenic diet for a long time the diabetogenic factor activity appears. The direct dependence between the level of the diabetogenic factor activity and the degree of the anticoagulating system depression caused by long keeping of the animals on the atherogenic diet has been revealed.

Animals↗
PubMed1986

[Role of the diabetogenic factor in hypercoagulation of the blood].

I.v. injection of the diabetogenic factor induced disfunction of anticoagulation system in rats. The endogenous heparin concentration decreases in the blood and no proper defensive response to thrombosis provocation occurs. The diabetogenic factor seems to play an important role in the development of thrombosis and other complications in diabetes.

Alloxan↗
PubMed1984

[Role of heparin in the realization of the hypoglycemic action of insulin].

The presence of reactive heparin in blood circulation is necessary for realization of the hypoglycemic action of insulin. This is confirmed by the fact that after heparin binding by protamin sulfate both endogenous and exogenous insulin do not exhibit any hypoglycemic activity. In animals with different basal concentration of heparin in the blood, the blockade of insulin action is attained by application of different doses of protamin sulfate, respectively. Based on the data obtained one can determine an approximate blood heparin concentration necessary for realization of the hypoglycemic action of insulin.

Animals↗
PubMed1984

[Diabetogenic action of alloxan in short-term termination of the blood supply to the pancreas and spleen].

It has been shown that the development of alloxan diabetes in rats and the appearance of diabetogenic factor in blood is caused by the direct alloxan action on pancreas and spleen--the organs supplying by blood through the spleen artery. The stopping of blood circulation in that artery preserves rat's organism from the development of general toxic effect of alloxan. The inactivation of alloxan as a diabetogenic agent has been shown after its 5-minute at 37 degrees C incubation with blood. It has been established that the half activity of intravenous injected alloxan disappears in rat's organism during 50 s. and does not depend on alloxan sensitivity of animals.

Alloxan↗
PubMed1983

[Electron microscopic study of the depolymerization process on unstabilized fibrin as affected by urea or monochloracetic acid].

With the help of the electronmicroscopic method the non-stabilized fibrin depolymerization has been studied. It has been established that under the action of urea or monochloridacetic acid the gradual transition of fibril clot's structure in globular fibrinolike material takes place. These globules have morphological likeness with the fibrin-monomer molecules and have analogy of the morphological properties to the non-stabilized fibrin dissolution products by complex compounds of heparin. The elimination of urea or monochloridacetic acid from media gives possibility to reconstruct the fibrillar fibrin structure.

Acetates↗
PubMed1982

[Hormonal dependence of the initial stages of heparin clearance during immobilization stress in the rat].

The 30-min immobilization stress reduces intensity of initial stages of heparin clearance in rats due to increased secretion of ACTH: in blockade of ACTH release the intensity of heparin clearance is not reduced whereas in intensifying the immobilization stress with ACTH administration it is reduced more than in immobilization alone. The stress does not accelerate heparin clearance in adrenalectomized animals. Substitutional administration of hydrocortisone normalizes the clearance in these animals. This suggests a permissive role of glycocorticoids in regulation of heparin clearance intensity. Detainment of heparin in the blood stream in stress is causally related to activation of anticoagulating system and to increased non-enzymatic fibrinolytie activity of the blood due to intensified formation of complex heparin compounds.

Adrenalectomy↗
PubMed1981

[Distribution of heparin and its complex compounds in the tissues of animals maintained on an atherogenic diet following intravenous administration of a thromboplastin-heparin complex].

After intravenous infusion of the thromboplastin-35- S-heparin complex into rats, maintained on the atherogenic diet within a prolonged period, distribution of the label in the animal tissues and its clearance were studied; total and non-enzymatic fibrinolytic activities were estimated. Inhibition of functions of the anticoagulation system, caused by long-term atherogenic diet in the animals, led to inhibition of the initial steps of heparin clearance as well as to alteration of the glycosaminoglycan distribution in various tissues. At the same time, formation and accumulation of heparin complexes as well as the non-enzymatic fibrinolytic activity were decreased in some tissues.

Animals↗
PubMed1980

[Tissue fibrinolytic activity of different sections of the heart in sympathectomized animals].

In the heart of intact rats aged 6 and 10 weeks the activity of nonenzymatic fibrinolysis was found to be maximum in the auricular tissue. In partly sympathectomized (destruction of 75% of neurons in the ganglia) 10-week-old rats fibrinolytic activity was sharply reduced in the auricular tissue, and in the atrial and ventricular myocardium. The content of the plasminogen activator in all parts of the heart decreased to zero value. In stress situations 50% of the rats die from thrombi in the atrial cavity. In partly sympathectomized 10-week-old rats (characterized by restoration of peripheral sympathetic innervation) the studied parameteres were normalized. The fibrinolytic potential of the heart tissue was markedly decreased in totally sympathectomized rats (destruction of more than 99.5% of the neurons); under the effect of stress 80% of these animals died.

Animals↗
PubMed1978

[Ultrastructure of unstabilized fibrin].

The structure of non-stabilized fibrin was studied by electron microscopy. Non-stabilized fibrin was shown to consist of a network of fibers (fibrils, from 2 to 10 mu in length, and up to 200 A in width). Negative contrasting with uranyl-acetate demonstrated non-stabilized fibrils to be made up of 5 to 10 longitudinally striated protofibrils and to be characterized by transverse striations with the main period of about 200 A. Comparison of the ultrastructure of stabilized and non-stabilized with factor XIIIa fibrin fibers demonstrated their morphological affinity.

Animals↗
PubMed1978

[Electron microscopic study of the products from dissolving unstabilized fibrin with complex heparin compounds].

Effects of some heparin complex compounds (heparin-urea, adrenaline-heparin, fibrinogen-heparin complexes and secondary complex adrenalin-heparin-fibrinogen) on factor XIIIa unstabilized fibrin were studied using electron microscopy. Fibrillar network of unstabilized fibrin destroys with the formation of globular molecular particles similar to fibrinogen molecule or fibrin monomer ultrastructure. A mechanism of fibrinolytic action of all the complexes mentioned is probably the same, since under dissolving of unstabilized fibrin, structures are found, which are similar to those forming under dissolving of unstabilized fibrin with urea.

Chemical Phenomena↗