Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA195

Poster Communications

The magnitude of compression-induced hyperaemia is affected by the driving pressure, more than by the muscle pump.

S. Roatta1, A. Messere1, R. Pertusio1, L. Ermini1, D. Maffiordo2, W. Franco2, C. Ferraresi2

1. Neuroscience, University of Torino, Torino, Italy. 2. Mechanical and aerospace engineering, Politecnico di Torino, Torino, Italy.

A short-lasting muscle compression (MC), as can be achieved by rapidly inflating and deflating a pneumatic cuff wrapped around a limb, is known to elicit a rapid and transient increase in blood flow to the affected tissues. The determinants of such compression-induced hyperaemia are still largely unknown. The observation that a larger response takes place if the limb is held below as compared to above heart level supports the involvement of the muscle pump (Credeur et al., 2015). On the other hand, other studies have argued against this hypothesis (Jasperse et al 2015). Aiming to identify the determinants of the compression-induced hyperaemia, this study investigates the effects of modulating the pressure levels that precede (pre-compression) and follow (post-compression) the MC stimulus, as a mean to affect vascular filling and perfusion pressure, respectively. In order to deliver the intended pressure profiles, a new a pneumatic system was developed and tested In 10 healthy subjects, haemodynamic changes were recorded in response to the MC stimulus (200 mmHg, 1-s duration) preceded or followed by pre- and post- compressions in the range 0-50 mmHg, and 50-s duration. The subjects sat on a chair with the leg extended horizontally, laying on a pillow. The haemodynamic response to MC was assessed by recording both the arterial inflow and venous outflow, by Doppler echography at the level of the femoral artery and vein, respectively. The magnitude of the hyperaemic response was quantified as the excess blood volume supplied to the lower leg during the hyperaemia (time integral of blood flow increase over the duration of the hyperaemia), while the displaced blood volume was measured as the time integral of venous blood flow over the duration of the MC. Increasing the pre-compression level from 10 to 50 mmHg progressively reduced the venous blood volume displaced by the MC, (by 70 ± 16 % at 50 mmHg, P<0.05), as compared to the MC without pre-compression. However, the magnitude of the hyperaemic response to MC (excess blood volume = 48.8 ± 14.1 ml) was not affected by pre-compression at any of the tested pressure levels. On the contrary, the hyperaemic response was progressively and strongly reduced by the application of post-compressions (by 85 ± 18 % at 50 mmHg, P<0.05), A new pneumatic prototype has been developed and validated allowing to deliver customizable compressive stimuli with pre-and post-compressions of adjustable pressure level. As expected, pre-compression reduced vascular filling, as indicated by the decrease in displaced blood volume, thus reducing the efficacy of the muscle pump. The independence of the hyperaemic response to MC on pre-compression level indicates a negligible role of the muscle pump. On the contrary, its strong dependence on the post-compression level suggests that changes in driving pressure are a major determinant of compression-induced hyperaemia.

Where applicable, experiments conform with Society ethical requirements