[Endothelium-dependent vascular response in rabbits during prolonged experimental hypercholesterolemia]. / Endotelii-zalezhni sudynni reaktsii u krolykiv pid chas tryvaloi éksperymentalnoi hiperkholesterynemii.

It was shown in experiments on anesthetized rabbits that disturbances in endothelium-dependent relaxant (Ach-induced) and constrictor (hypoxia-induced) vascular responses depended on duration of high hypercholesterol diet and on the structural damage of the vascular wall as well as on changes in the functional activity of endotheliocytes. Short (1 month) hypercholesterolemia led to thickening of the blood-cellular barrier and promoted a decrease in the endothelium-dependent relaxant response to Ach. At the same time short hypercholesterolemia enhanced a constrictor component of the vascular smooth muscle (VSM) response to hypoxia. It may be explained by a different degree in disturbance of synthesis and/or release of the endothelial relaxing and constrictor factors. At the later period of hypercholesterolemia (2-9 month) parallel with a pronounced damage of the endothelium and development of atheromatous plaques, the impairment of the endothelium-dependent vascular responses became more and more pronounced. As a rule, Ach-induced relaxation in VSM was registered in sole experiments only and very often was either absent or transformed to contraction. Constrictor components of vascular response to hypoxia were significantly decreased as well. The above-mentioned disbalance between endothelial relaxant and constrictor factors in combination with structural damage of the endothelium and difficulty in transendothelial transport of these factors to effector elements of the vascular wall may cause vasospastic reactions in VSM at atherosclerosis.

[The role of the endothelium in the development of functional hyperemia of the skeletal muscles]. / O roli éndoteliia v razvitii funktsional'noi giperemii skeletnykh myshts.

Experiments on anesthesized dogs demonstrated that gastrocnemius muscle vessels working hyperemia substantially decreased after chemical destruction of endothelium by saponin, inhibition of endothelium-derived relaxing factor synthesis by gossypol and inhibition of quanylate cyclase by methylene blue. Reaction was not decreased after cyclooxygenase inhibition by indomethacin. The endothelium-derived relaxing factor predecessor--L-arginine essentially increased working hyperemia. We concluded that endothelium plays an important role in reaction of working hyperemia by endothelium-derived relaxing factor release.