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

• Published in: Clinical physiology and functional imaging Vol. 26; no. 2; pp. 132 - 137
• Main Authors: Charles, Marc, Pichot, Vincent, Barthelemy, Jean-Claude, Roche, Frederic, Costes, Frederic
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.03.2006; Blackwell Science
• Subjects: Adult; Biological and medical sciences; Exercise - physiology; Forearm - blood supply; Fundamental and applied biological sciences. Psychology; Hemodynamics. Rheology; Humans; Hyperemia - physiopathology; Ischemia - physiopathology; Lower Body Negative Pressure; Male; metabolic vasodilatation; Regional Blood Flow; Supine Position; Sympathetic Nervous System - physiology; sympathetic vasoconstriction; Tachycardia - physiopathology; Vascular Resistance - physiology; vascular sympathetic escape; Vertebrates: cardiovascular system; Human; Vasoconstriction; Cardiovascular disease; Smooth muscle; Negative pressure; Metabolism; Sympathetic nervous system; Reactive hyperemia; metabolic vasodilatation; Vasomotricity; Autonomic nervous system; sympathetic vasoconstriction; Arterial hypotension; Upper limb; Muscular tonus; vascular sympathetic escape; Adaptation
• ISSN: 1475-0961; 1475-097X
• DOI: 10.1111/j.1475-097X.2006.00665.x

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.