[The role of the endothelium in the local vascular reactions of the skeletal muscles].

Chemical de-endothelialization of the m. gastrocnemius' vessels nearly completely blocked the working, reactive and postelongation hyperemia as well as the hyperemia induced with augmentation of the amplitude of intra-vessel pressure pulses. Endothelium seems to take part in the above responses through effects upon the vessels' smooth muscles of a vasodilatory substance released or synthesized by the endothelial cells in the mechanical deformation.

[The effect of arterial pressure pulsations on the resistive function of the vessels in different organs and species and with differing initial tonus].

In normotensive rabbits, normo- and hypertensive rats, an increase of the pulse amplitudes from 0-10 to 70-80 mm Hg at a constant value of the mean pressure in magistral arteries in the skeletal muscles and skin, induced a decrease of the resistance against blood flow due to occurring vasodilation. The response in the SHR was considerably lesser than in normotensive animals. The vasodilation occurring in some organs and tissues to dynamic deformation of the blood vessels by the pulse pressure seems to play a significant role in the adaptive responses of the circulation system to ambient stimuli activating the heart output.

[The effect of the amplitude and frequency of blood pulsations on the peripheral vascular tonus].

In acute experiments on cats, hindlimbs' skeletal muscles, small intestine, a lung's lobe or a kidney were perfused. The mean value of the perfusion pressure was constant. The increase in frequency of the perfusion pressure oscillations from 0.

[Blood supply of skeletal muscles in reactive hyperemia].

In 18 anesthetized cats, 60-sec occlusion of the m. gastrocnemius artery entailed a decrease in the muscle blood supply by 15-20 ml of the blood volume in the vessels whereas the post-occlusion increase in the blood flow restored the blood volume with 45% excess. The intravascular accumulation of the blood exerting a moderating effect upon the venous return while preserving the increased arterial inflow, can be regarded as an automatic way of limiting the hemodynamic excitation due to the postocclusion shifts and involved in systemic circulation.