[Antiatherogenic characteristics of korvitin: effect on proteasome activity of the aorta, heart, and blood cells].

We studied the changes in proteasomal proteolisis during modelling of rabbit cholesterol-induced atherosclerosis. It was determined that in aorta the TL activity of proteasome increased 2.4-fold (P < 0.05), CTL activity increased by 43%, and PGPG--by 10%. In heart tissue it was observed the increase of CTL proteasome activity by 14%. The application of "Korvitin" (water-soluble form of quercetine) followed by considerable decrease of proteasomal activity both in tissues (aorta and heart) and leucocytes. The intensity ofatherosclerotic changes in aorta was significantly smaller. Obtained data suggest that "Korvitin" reveales angioprotective properties mediated by it effect on proteasomal proteolisis.

[Proteasome activity changes in the aorta, heart tissues, and blood leucocytes in modelling of cholesterol atherosclerosis].

In experiments on modelling of cholesterol atherosclerosis in rabbits (1% cholesterol-rich diet during 2 month) it was determined changes of trypsin-like (TL), chymotrypsin-like (CHTL) and peptydilglutamilpeptidase (PGPG) proteasomal activity in tissues of aorta, heart and isolated blood leukocytes. It was shown that cholesterol-rich diet caused significant increase of TL (3.2 fold, P=0.003), PGPG (1.8 fold, P=0.003) proteasomal activity in aorta tissues, and PGPG activity (1.8-times, P=0.003) in myocardium. In isolated blood monocytes, the CHTL and PGPG activities were significantly increased (1.9 fold, P=0.05 and 11.6 fold, P=0.0001, respectively) and in PMN leucocytes the PGPG activity of proteasome was also significantly increased (1.8 fold, P=0.031). Proteasomal activity in lymphocytes during cholesterol atherosclerosis modelling had no significant changes. The data obtained indicate that alimentary hypercholesterolemia induces considerable changes of proteasomal activity in cardio-vascular system and blood cells that take part in atherogenesis.

[Elastolytic system of the pancreas in modelling diabetes mellitus]. / Stan elastolitychnoï systemy pidshlunkovoï zalozy pry modeliuvanni tsukrovoho diabetu.

At modelling streptozotocin and alloxan diabetes mellitus in rats we have detected an imbalance between elastase and its inhibitors (alpha 1 inhibitor of protein kinases, alpha-2 macroglobulin, acid-thermoresistant inhibitors) in tissues of the pancreas. The contribution of proelactase decreased but that of an active form of protein kinase increased; the content of alpha 1 inhibitor of protein kinase and alpha 2 macroglobulin reduced, however, the contribution of the acid-thermoresistant inhibitors in the pancreatic tissues increased. Imbalance in the system elastase-inhibitors, shown at the model of diabetes mellitus, may be an important mechanism of an exocrine insufficiency of the pancreas which results in pancreatitis.

[Effect of acid-base imbalance on the equilibrium of elastase and its inhibitors in rat serum and aorta tissues]. / Vplyv porushen' kyslotno-luzhnoho stanu na balans elastazy ta ïï inhibitoriv u syrovattsi krovi ta tkanynakh aorty shchuriv.

In experiments on the acid-base imbalance modelling (acidosis induced with either lactate or ammonium chloride alcalosis induced with sodium hydrocarbonate) in rats, there were studied elastase activity, alpha-2-macroglobulin and alpha-1 proteinase inhibitor contents in blood serum and tissues of the aorta. The results obtained indicated that, in the models of both acidosis and alcalosis an disbalance between elastase and its inhibitors was observed. However, in NH4CL-acidosis in homogenates of aorta the inhibitors/elastase coefficient decreased at the expense of a reduction in contents of alpha-2-macroglobulin, while in lactate-acidosis it only decreased at the expense of an increase in elastase activity. In alcalosis, contents of proteinase inhibitors were even increased, however a substantial increase in elastase activity indicated a reduction in integrative coefficient. Similar changes were observed in blood serum, except elastase activity was considerably elevated in NH4CL-acidosis and did not change in lactate-acidosis. Thus, an disbalance in the elastolytic system associated with different types of acid-base imbalance can promote the destruction of elastic fibers of aorta, which is considered as one of initial mechanisms in pathogenesis of arteriosclerosis.

[Activity of elastase and its inhibitors in tissues of aorta and blood serum in various types of acidosis]. / Aktyvnist' elastazy ta ïï inhibitoriv u tkanynakh aorty ta syrovatsi krovy pry riznykh vydakh atsydozou.

In modeling of different types of acidosis (hyperchloraemic, lactate and ketoacidosis in the starvation) at rats the elastase activity, contents of alpha-2 macroglobulin (alpha 2M) and alpha-1 proteinase inhibitor (alpha 1PI) in aorta tissues and blood serum were studied. The obtained results indicate that the degree of disturbance in system elastase-inhibitors depends on expressiveness of parameters changes in system of acid-base state regulation. In modeling of various types of acidosis coefficient inhibitors/elastase is reduced due to different parameters change in aorta, namely decrease of alpha 2M contents--in hyperchloraemic acidosis, increase of elastase activity--in lactat-acidosis, increase of elastase activity and decrease of alpha 2M contents--in ketoacidosis. In blood serum the similar coefficient is reduced due to increase of elastase activity and decrease of alpha 2M contents in hyperchloraemic acidosis and starvation, and, in turn, due to decrease of alpha 2M contents--in lactat-acidosis. The obtained data indicate that one of mechanisms of vascular wall damage in acidosis is disturbance of balance between elastase and its inhibitors in tissues of arteries.

[The current concepts of the pathogenesis of Mönckeberg-type arteriosclerosis]. / Suchasni uiavlennia pro patohenez arteriosklerozu menkeberhivs'koho typu.

On the basis of experimental researches the circuit of pathogenesis of Mönckeberg's arteriosclerosis--one of the most widespread types of arteriosclerosis is offered. The most important mechanisms realized during development of this pathological process, following: 1) actions of the injuring factor cause necrobiotic change of vascular wall cells; 2) activation of proteolytic enzymes, disturbance of balance between proteinases and their natural inhibitors results in destruction of extracellular matrix fibers and excessive stimulation by products limited proteolysis of vascular wall cell; 3) infringements of intracellular ion homeostasis at the expense of the mentioned below factors exhaust energy systems (last in case of metabolic poison action can be primary are damaged); 4) infringements in system of blood, in particular, in calcium homeostasis, blood coagulation, lipid spectrum promote additional damage of vascular wall cells; 5) dystrophic and metastatic calcification of media; 6) development "unspecific mesenchymal reaction", including fibrosis and sclerosis, in damage zone of vascular wall.

[The role of the calcium-accumulating capacity of the intracellular reserves in the smooth muscles of the blood vessels in the development of their catecholamine-related damage]. / Doslidzhennia roli kal'tsiiakumuliuiuchoï zdatnosti vnutrishn'oklitynnykh zapasnykiv hladen'kykh m'iaziv krovonosnykh sudyn u rozvytku ïkh katekholaminovoho poshkodzhennia.

Noradrenaline (10(-5)M) contractile reactions of smooth muscles of the rabbit arteries and veins (aorta, a. femoralis, V. cava posterior, v. femoralis) were investigated in the calcium-free medium using different methods of loading (0.5 mM Ca2+; 0.5 mM Ca2+; 60 mM K+; 20 mM Ca2+) of their predepleted noradrenaline-sensitive intracellular calcium stores. The comparative analysis of indices of relationships of maximum amplitudes using 0.5 mM Ca2+ in presence of 60 mM K+ and 0.5 mM Ca2+, 20 mM Ca2+ and 0.5 mM Ca2+ has shown that calcium-accumulating ability of vein stores exceeds significantly that in arteries independent of the loading source. The toxic concentration of adrenaline (50 mg/kg in ear vein everyday during 5 days) inhibited more significantly the ability of arterial calcium stores to absorb cytoplasmic but not extracellular calcium. We failed to find the changes of the kind in veins. It has been found that the phenomena described are very important as they show different resistance of arteries and veins to the calcium injury.

[Energy metabolism in arteries and veins in modelling epinephrine damage to the vascular wall]. / Energeticheskii obmen v arteriiakh i venakh v usloviiakh modelirovaniia adrenalinovykh porazhenii sosudistoi stenki.

Experiments were conducted on rabbits to study some indices of energy metabolism in arteries and veins under conditions of chronic epinephrine intoxication. Reduced intensity of oxygen consumption, increased intensity of lactic acid production, and reduced content of macroergic phosphates (ATP, phosphocreatine) were revealed in the walls of the arteries studied. Disorders of energy metabolism in veins were either less marked (portal vein) or absent (vena cava posterior). The revealed decrease of the intensity of energy metabolism in the arterial wall is considered to be among the possible mechanisms of the development of Monckeberg's arteriosclerosis.

[Effect of acute tuberculous intoxication on the intensity of energy metabolism of the vascular walls in rabbits]. / Vliianie ostroi tuberkuleznoi intoksikatsii na intensivnost' energeticheskogo obmena v stenke krovenosnykh sosudov krolikov.

Acute tuberculous intoxication in rabbits was accompanied by impairment of energy metabolism in the vessel walls: lower intensity of oxidative processes and higher activity of glycolysis. In the arteries which are vessels highly sensitive to sclerotic affections the observed metabolic disorders were much more pronounced than in the veins which are vessels resistant to angiosclerosis.