[Reaction of osseous tissue and the osteoclast population in rats to biphosphonates and vitamin D3 under conditions of hypokinesia]. / Reaktsiia kostnoi tkani i populiatsii osteoklastov krys na bisfosfonaty i vitamin D3 v usloviiakh gipokinezii.

Oral administration of hydroxy-dimethyl aminopropylene biphosphonate (DMAP) at a dose of 0.5 mg/kg increased the volume density (mass) of trabecular bone in the tibial metaphysis of untreated rats and helped to maintain it at the normal level in hypokinetic rats. Oral administration of hydroxy-ethylidene biphosphonate (OEDP) at a dose of 20 mg/kg and vitamin 24,25(OH)2D3 at a dose of 1,25 micrograms did not induce any quantitative changes in bones of untreated or immobilized rats. The combined treatment with either biphosphonate and vitamin D3 exerted a similar effect as compared to that of biphosphonates used singly. During hypokinesia the total amount of osteoclasts declined. This effect was also seen in response to biphosphonates and vitamin D3. The two biphosphonates produced an opposite effect on the osteoclast population in untreated animals: it increased in response to OEDP and decreased in response to DMAP. In contrast to OEDP, low doses of DMAP can efficiently inhibit bone resorption upon various routes of its administration and can be viewed as a preventive and therapeutic drug in the case of osteoporosis.

[Dynamics of immobilization-induced osteoporosis in rats]. / Dinamika immobilizatsionnogo osteoporoza u krys.

Wistar male rats weighing 250-270 g were exposed to hypokinesia for 7, 15, 35 or 60 days. Spongy bone of the metaphysis of long bones, vertebral body, breast bone and iliac bone were examined histomorphometrically. It was found that during hypokinesia osteoporosis developed in two stages: Stage 1 (from hypokinesia day 1 to day 15) was characterized by a drastic bone mass loss due to stress-effects (steroid osteopenia) and Stage 2 (from hypokinesia day 15 to the end) was characterized by adaptive changes which included steady-state development and transition to a lower functional level (immobilization osteoporosis).

[Effect of hirudin on hormonally caused activation of nonenzymatic fibrinolysis in immobilization stress]. / Deistvie girudina na gormonal'no obuslovlennuiu aktivatsiiu nefermentativnogo fibrinoliza pri immobilizatsionnom stresse.

The specific inhibitor of thrombin-hirudin was used for studying the mechanism of activating effect of ACTH and adrenaline upon the unenzymatic fibrinolysis (UEF), the latter characterizing the function of the anticoagulating system (ACS). Simultaneous administration of ACTH and hirudin to animals subjected to the immobilization stress did not reduce the effect of ACTH upon UEF, while simultaneous administration of adrenaline and hirudin revealed a diminished effect of the former. This suggests different mechanisms of ACTH and adrenaline effects upon UEF: the stimulating effect of noradrenaline is realized through thrombinogenesis followed by activation of the ACS function and by an increase of UEF and therefore inhibitable by hirudin which form an inactive complex with thrombin. While the stimulating effect of ACTH upon UEF is exerted, apparently, not through thrombinogenesis and hence is valid even in presence of hirudin. Hirudin proper exerts no effect upon UEF.