Continuous control of the lumen of feline conduit arteries by blood flow rate.

Dilatation of conduit arteries induced by increased blood flow was studied in feline femoral, common carotid, or renal arteries. The outer diameter of the arteries perfused under stabilised transmural pressure conditions was continuously measured with a contact capacitance type transducer. A rise in blood flow rate was shown to induce arterial dilatation, the magnitude of which depended linearly on the extent of flow increase over a wide range of flow rates (usually from 10-15 to 35-50 ml.min-1). Increase in flow above this range caused a smaller increase in diameter followed by a plateau phase. The maximal (mean(SEM] flow induced increase in arterial diameter was 25.8(2.8)% for the femoral, 25.5(2.2)% for the common carotid, and 24.6(5.1)% for the renal artery. This dilatation almost completely compensated for the increase in flow, causing a practically unchanged pressure difference along the arteries. A pronounced dilator response to an increase in blood flow rate as small as 1 ml.min-1 could be recorded for all flow rates where the diameter-flow relation was linear. Flow induced dilatation persisted during perfusion with a solution free of vasoactive substance. Thus in the arterial wall some mechanism provides effective continuous control of the lumen and, consequently, hydraulic resistance of the arteries in response to increases in blood flow.

Flow-induced control of arterial lumen.

Blood flow velocity is a factor that affects the diameter of arteries. In order to investigate the flow-induced arterial dilatation, the outer diameter of the femoral, common carotid or renal arteries of anaesthetized cats was measured during perfusion of these arteries with blood or plasma-substituting solutions under conditions of stabilized perfusion pressure. It has been shown that, whatever the perfusate, blood or a substituent, an increase in flow makes the artery to dilate. Consequently, the flow-induced dilatation is not due to any blood-borne humoral factor. As an increase in the solution's viscosity causes dilatation even at constant flow-rate and pressure in the artery, the effect is to be ascribed to the ability of the vascular wall to perceive shear stress. As far as removal of endothelium eliminates the dilatation evoked by increasing flow or fluid viscosity, it may be concluded that the flow-induced dilatation is due to the sensitivity to shear stress of the endothelium.

[Regulation of the femoral artery diameter during changes in the rate of flow of perfusion solutions]. / Reguliatsiia diametra bedrennoi arterii pri izmeneniiakh skorosti techeniia perfuzionnykh rastvorov.

It was shown in acute experiments on cats that the femoral artery under constant pressure in its lumen changes its diameter in response to variations in the velocity of both the blood and perfusion solutions. This permits the conclusion that chemical factors of the blood are not responsible for dilatation reactions of the large arteries which appear in response to the increases in the flow rate.

[Effect of distribution of the stimulation frequency in the volley on post-contraction hyperemia of the gastrocnemius muscle of cats]. / Vliianie raspredeleniia chastoty razdrazhaiushchikh stimulov v zalpe na rabochuiu giperemiiu ikronozhnoi myshtsy koshek.

The influence of stimulation frequency distribution in a volley on postexercise (postcontraction) hyperemia was studied in acute experiments on cat gastrocnemius muscle. The initial high frequency of the rhythmic volley augmented the postcontraction hyperemia indices (the peak blood flow and an additional blood volume).

[2 phase of the working hyperemia of skeletal muscle]. / Dve fazy rabochei giperemii skeletnoi myshtsy

The dynamics of the working hyperemia of cat m. gastrocnemius was studied by means of an electromagnetic flowmeter. Two phases could be distinguished in the increase in the rate of circulation. There proved to be a rapid increase of the blood flow during the I phase, and an abrupt reduction of this process during the II phase. The duration of the I phase failed to depend on the frequency of stimulation and on the number of the contracting motor units. The II phase was absent when the number of the contracting motor units was few or the frequency of stimulation was low. It is suggested that the dilatation of the precapillary arterioles is responsible for the I phase of the working hyperemia and the II phase is connected with the dilatation of the larger arteries.