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Forelimb postischaemic reactive hyperaemia is impaired by hypotensive low body negative pressure in healthy subjects

Authors

  • Marc Charles,

    1. Research Unity ‘Physiology Physiopathology of Exercise and Handicap’ and CHU Saint-Etienne, North Hospital, EFCR Unity, University Jean Monnet, Saint-Etienne Cedex 2, France
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  • Vincent Pichot,

    1. Research Unity ‘Physiology Physiopathology of Exercise and Handicap’ and CHU Saint-Etienne, North Hospital, EFCR Unity, University Jean Monnet, Saint-Etienne Cedex 2, France
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  • Jean-Claude Barthelemy,

    1. Research Unity ‘Physiology Physiopathology of Exercise and Handicap’ and CHU Saint-Etienne, North Hospital, EFCR Unity, University Jean Monnet, Saint-Etienne Cedex 2, France
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  • Frederic Roche,

    1. Research Unity ‘Physiology Physiopathology of Exercise and Handicap’ and CHU Saint-Etienne, North Hospital, EFCR Unity, University Jean Monnet, Saint-Etienne Cedex 2, France
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  • Frederic Costes

    1. Research Unity ‘Physiology Physiopathology of Exercise and Handicap’ and CHU Saint-Etienne, North Hospital, EFCR Unity, University Jean Monnet, Saint-Etienne Cedex 2, France
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Marc Charles, CHU Saint-Etienne, North Hospital, EFCR Unity, 42055 Saint-Etienne Cedex 2, France
E-mail: marc.charles@univ-st-etienne.fr

Summary

Local metabolic conditions adapt blood supply to metabolic requirement by a direct effect on vascular smooth muscles and indirectly by modulating sympathetic vasoconstrictor effectiveness. During exercise, sympathetic nervous activity could in turn interfere on local metabolic control of vascular tone and restrain blood flow to active muscles. In order to investigate that interaction non-invasively, we measured postischaemic reactive hyperaemia (RH) in the forelimb of eight healthy young men (22·7 ± 2·1 years) at rest and during two levels of sympathetic stimulation using low body negative pressure (LBNP −15 and −30 mmHg). During every stages, RH was measured after 40, 60, 90 and 180 s of arterial occlusion, respectively. In control conditions, RH rose with duration of ischaemia (18·9, 24·2, 30·4, 33·1 ml min−1 per 100 ml−1 for 40, 60, 90 and 180 s of ischaemia, respectively). During non-hypotensive LBNP (−15 mmHg) sympathetic activation was associated with decreased forelimb blood flow (6·4 ± 0·9 versus 3·9 ± 0·6 ml min−1 per 100 ml−1, P<0·01), but RH were not significantly different from control conditions. During hypotensive tachycardia LBNP (−30 mmHg), RH were significantly lower than under the previous LBNP stage. This fall in RH was greater after the shortest gap of ischaemia and tapered off as arterial occlusion gap increased (−22·3, −13·1, −10·5 and −8·7% for 40, 60, 90 and 180 s of ischaemia, respectively). These results suggested that vascular tone adaptation to local metabolic conditions was modified by sympathetic nervous activation. This was particularly marked when an hypotensive-mediated sympathetic stimulation was opposed to short gaps of ischaemia.

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