[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.

[Changes in the total calcium content and in the activity of alkaline phosphatase and gamma-glutamyltransferase in the blood serum of rats with Mönckeberg's experimental arteriosclerosis]. / Zminy vmistu zahal'noho kal'tsiiu, aktyvnosti luzhnoï fosfatazy i hamma-hlutamiltransferazy v syrovati krovi shchuriv pry eksperimental'nomu arteriosklerozi Menkeberha.

Experiments on rats (single-action, six-days' hyperepinephrinemia and monoiodacetatic acid intoxication) were performed to study the calcium concentration, alkaline phosphatase and gamma-glutamyltransferase activities in serum at Monckeberg's medial calcific sclerosis modelment. It is established reduction serum level of calcium in an hour past single-acting hyperepinephrinemia, increase it's level after six-days'-monoiodacetatic intoxication, increase of "serum alkaline phosphatase activity/gamma-glutamyltransferase activity" (as indirect evidences the bone isozyme of alkaline phosphatase and parathyroid hormone activity increase) after six-days' hyperepinephrinemia and monoiodacetatic acid intoxication. Probably, these changes in serum calcium metabolism and system it's regulation may play pathogenetic role in early period Mönckeberg's arteriosclerosogenesis.