Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB185

Poster Communications

Tissue oxygenation: a novel modulator of compression-induced hyperaemia

A. Messere1, M. E. Tschakovsky2, S. Seddone1, W. Franco3, D. Maffiordo3, C. Ferraresi3, S. Roatta1

1. Neuroscience, University of Torino, Torino, Italy. 2. School of Kinesiolo, Queen's University, Kingston, Ontario, Canada. 3. Mechanical and aerospace engineering, Politecnico di Torino, Torino, Italy.

Skeletal muscle vasculature exhibits a rapid dilatation in response to mechanical compression (MC), that leads to transient hyperaemia. This hyperaemia is markedly attenuated in response to a second stimulus delivered within a short time (2 min) from the first (Messere et al., 2017). Indirect evidence suggests that the increase in tissue oxygenation developing during the first hyperaemia could be responsible for attenuating further hyperaemic responses. Alternatively, the effect could be mediated by transient inactivation of the mechano-sensitive structures underlying the rapid dilatation. Aim of this study was to test the hypothesis that a prior hyperaemia and ensuing increase in tissue oxygenation is necessary for the attenuation of MC-induced hyperaemia. In 8 healthy subjects two MCs separated by a 25-s interval were delivered to the forearm by means of a pneumatic cuff. The sequence was performed a second time after a resting interval of at least 5 min. In one of the sequences (randomly selected) the hyperaemic response to the first MC was prevented by partial occlusion of the axillary artery. Tissue oxygenation from forearm muscles and brachial artery blood flow were continuously monitored by means of Near Infrared Spectroscopy (NIRO 200, Hamamatsu) and Doppler-echography (MyLab 25, Esaote), respectively. The magnitude of the hyperaemic response was quantified as the excess blood (in ml) supplied to the forearm during the hyperaemia. In the absence of blood flow restriction, the hyperaemic response to the first MC was 14.8 ± 3.9 ml (P<0.05), which was followed by a slower increase in tissue oxygenation from 65.2 ± 4.7 % to 76.5 ± 3.8 % (P<0.01), remaining significantly elevated at the time of delivery of the second MC (75.3 ± 4.2 %, P<0.05). In this condition the hyperaemic response to the second MC was markedly attenuated: 5.7 ± 3.3 ml (P<0.05). When the hyperaemic response to the first MC was prevented, tissue oxygenation did not increase (64.9 ± 4.9 %) and the magnitude of the hyperaemic response to the second MC did not exhibit attenuation (14.4 ± 3.9 ml). In conclusion, the present study demonstrates that the putative inactivation of mechano-sensitive structures upon the first MC is not responsible for the attenuation of the rapid hyperaemia in response to the second MC. Conversely the development of prior hyperaemia is a necessary condition for the attenuation to take place and tissue oxygenation appears to by a major modulator of the rapid dilatation. In addition, these results support the concept that tissue hyper-oxygenation is a key signal in the regulation of muscle blood, activating a prompt and effective action against hyper-perfusion (Golub & Pittman 2013) and may have relevance for investigations and treatments in which mechanical stimuli are delivered to improve muscle perfusion.

Where applicable, experiments conform with Society ethical requirements