The morphological properties of the blood thrombocytes in bronchial asthma patients before and after thrombocytapheresis. / Morfologicheskie svoistva trombotsitov krovi u bol'nykh bronkhial'noi astmoi do i posle trombotsitafereza.

Morphological characteristics of platelets were assessed electron microscopically in 15 patients with atopic and aspirin bronchial asthma (BA) before and after thrombocytapheresis (TA). All the patients had a definite shift of platelet subpopulations to greater percentage of spherical forms as well as defects in cell ultrastructure. This makes evident platelet activation in patients with BA aggravation. TA entails a positive trend to normalization of platelet subpopulations and cytoskeleton. The ability to normalize platelet morphofunctional status determines its clinical effectiveness in bronchial asthma.

[The possible role of the inner mitochondrial membrane in regulating oxidative phosphorylation in cells in vivo]. / O vozmozhnoi roli vneshnei membrany mitokhondrii v reguliatsii okislitel'nogo fosphorilirovaniia v kletkakh in vivo.

It has been shown for the first time that the outer mitochondrial membrane has a low permeability for ADP and can control its diffusion into cells in vivo. Respiration of saponin-skinned cardiac and skeletal muscle fibers is maximally stimulated by millimolar concentrations of external ADP. The apparent Km values for ADP are equal to 297 +/- 35 and 334 +/- 54 microM, respectively. After complete extraction of myosin with 0.8 M KCl, which fully preserves the intact structure of the mitochondria, the apparent Km values for exogenously added ADP does not change. However, disruption of the outer mitochondrial membrane by osmotic shock (treatment with 40 mOsM KCl) causes a reduction of the apparent Km value down to 32.3 +/- 5.0 microM of ADP. The apparent Km for ADP in isolated heart mitochondria is 17.6 +/- 1.0 microM. It is concluded that there exists an intracellular factor in the cells in vivo which controls the outer mitochondrial membrane and notably decreases its permeability for ADP. After isolation of mitochondria this factor is lost. When mitochondrial creatine kinase is activated, weak intracellular fluxes of ADP passing through the outer mitochondrial membrane in the skinned fibers are amplified manifold due to the tight functional coupling between mitochondrial creatine kinase and the oxidative phosphorylation system. This coupling is considered to be the central mechanism in the control of cell respiration.

[Damage to human endothelial cells by cholestane-3 beta,5 alpha,6 beta-triol and the protective effects of preparations that raise the intracellular level of cAMP]. / Povrezhdenie éndotelial'nykh kletok cheloveka kholestan-3 beta,5 al'fa,6 beta-triolom i zashchitnye éffekty preparatov, povyshaiushchikh vnutrikletochnyi uroven' tsAMF.

Effect of drugs, which are able to elevate the intracellular level of cAMP, on resistance of human umbilical vein endothelial cells (HUVEC) to cholestane-3 beta,5 alpha, 6 beta-triol (Triol)-induced injury was studied. Triol at a concentration of 62 microM caused death of 50% of cells after a 24 hour incubation. Addition of forskolin (10 microM), methylisobutylxantine (100 microM), or 8-Br-cAMP (100 microM) into the incubation medium prevented injury of HUVEC under these conditions. These findings indicate that endothelial resistance to the injury can be regulated by the adenylate cyclase system. A comparative study on Triol-induced injury of adult human aortic endothelial cells isolated separately from zones of low (LP) and high (HP) probability of atherosclerosis was also performed. In 7 cases endothelial cells isolated from the LP zones were more resistant to Triol-induced injury, in 2 cases the differences were not significant. The development of atherosclerotic lesion in HP zones is likely to be associated with a higher sensitivity of endothelial cells from these zones to different injuring agents.