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Intraocular pressure (IOP) and eye hydrodynamics (aqueous outflow easiness rate (C) and moisture chamber production (F)) were studied in 9 adult volunteers subjected to the hypogravity effects of head-down tilt (HDT) at -15⁰ to the horizontal plane. The volunteers stayed in the horizontal and tilted positions for 10 minutes. IOP was measured according to Maklakov (tonometer 5 g), C and F - according to Nesterov (simplified tonography). In parallel, heart rate (HR) and systolic and diastolic blood pressures (SBP and DBP) were measured in the sitting, lying and tilted positions. In HDT IOP rose 10.3 % (p < 0.05) and C reduced 60 % (p < 0.05); F showed an uncertain trend down by 59 % (p > 0.05). Increase of the Bekker coefficient by 168 % (p < 0.05) could testify interconnection of the increased IOP and impaired moisture outflow. Moreover, in HDT DBP showed a rise while HR decreased. These results suggest that during brief tilt- down IOP increases not only because of a greater filling of the choroid vessels, but also because of retarded outflow of the intraocular fluid. The downward trend in fluid production can be a compensatory reaction to increased'IOP.

When modeling effects of hypogravitation by the method of hindlimb unloading in rats the area of cross-section in lumbar part of a spinal cord was found to reduce. The analysis of spinal cord slides showed that these changes are associated with a decrease in the area of white substance of a spinal cord. Data obtained are consistent with our previous observation of a decrease in expression of the genes encoding myelin proteins. Results of our researches give the good reasons to believe that miyelinization failure in CNS is one of the factors that underlie the development of hypogravitational motor syndrome.

Downsizing of muscle fibers, decline of their contractility and alteration of the myosin phenotype towards fast isoforms prevalence are ranked among the main consequences of gravitational unloading of postural muscles. Role of Ca2+ ions in these processes is the subject of the article. Authors revealed increase in the Ca2+ content in myofibers of resting m. soleus of mice following hindlimb suspension. It has been also reported earlier that nifedipine, a specific blocker of calcium L-channels, can prevent this increase acting on the central and local controls. Therefore, a supposition can be made that activation of the dehydropyridine Ca channels is responsible for Ca2+ rest accumulation during gravitational unloading. The calcium-dependent signaling pathways may be thought of as key players in a number of developments due to gravitational unloading. To begin with, already in early 1990s this role in the hypogravity-induced muscle atrophy was ascribed to calpains, Ca-dependent proteinases which was clearly demonstrated later. We observed maintenance of the relative titin and nebulin contents in unloaded m. soleus associated with the effect of Ca chelators. Also, nifedipine injection reduced significantly the growth of MHC fast isoforms expression during gravitational unloading equally on the RNA and protein levels. To bring to light the place of calcineurin/NFAT signaling system in the MHC phenotype alteration, we undertook inhibition of this pathway by injection of cyclosporine A. This resulted in getting evidence of the stabilizing function of this pathway as it opposes to the myosin phenotype transformation to the fast one.

Architectonics of the fibrillar actin in cultures of human endothelium cells (EC) during and after extended (144 hrs.) clinostatting was examined under the fluorescent microscope. In control EC cultures, F-actin was composed of a network of filaments located both in the center and along the periphery of cells. One hour of rotation did not visibly affect the actin skeleton, however, in two hours there were cells with filaments displaced toward the membrane. Twenty-four hours of rotation caused total remodeling of the cytoskeleton so that practically the whole population of thin filaments had migrated toward the periphery. In most of the cells the intercell contact area formed undulating edges rich in F-actin. A similar picture could be seen after 144 hrs. of rotation. The actin skeleton partially recovered in 4 hrs. and regained the normal structure in 24 hrs. of rehabilitation. Same period was required for cells to restore their structure completely following the extended clinostatting. These data suggest sensitivity of the EC cytoskeleton to changes in the gravity vector. Remodeling of the actin skeleton in a changed gravity is reversible and proceeds more rapidly than recovery.

Antiorthostaic hypokinesia (AOHK) was found to entail a considerable diminishing of the control system's precision abilities. In the first 14-30 days of the AOHK (the 1st stage), variability of interimpike intervals (ISI) was sharply increased as well as the degree of synchronisation of the motor units' (MU) activity; starting from the 30th day (the 2nd stage), a regular diminishing of the ISI occurred and the MU synchronisation disappeared. The data obtained suggest the different nature of the precision disorders during the 1st and the 2nd stages of the AOHK: a reflex responses to support unloading and the atrophic processes in the muscles, respectively.

Effects of long-term simulation of hypogravity on actin cytoskeleton and cell migration were investigated in cultured human endothelium cells (EC). In control, F-actin resided predominantly on the periphery of cell forming an array of parallel bundles with "dense bodies" along the edge. A small number of actin cable fibers was found in the center. Already after 1-2 hrs of clinostatting at 5 RPM the cell cytoskeleton showed actin filament thinning and displacement toward the cell edges. In subsequent 6-18 hrs, almost all actin fibers had left the center part of EC and had ranged themselves in a continuous F-actin line in the intercellular contact area. In most cases, these changes resulted in the so-called "ruff-edge". Since both the disappearance of cable fibers and formation of the "ruff-edge" add to the cell migration activity, this parameter was studied with the would-healing model. According to our data, 24-48 hrs of exposure to hypogravity stimulates cell migration and expedites 2-3 times reparation of mechanically damaged monolayer. The results suggest that effects of hypogravity on cultured human EC are likely to be consequent to alterations in the activity of protein kinase C and/or adenylate cyclase involving many members of the cellular metabolism.