Passive leg movement-induced hyperemia with a spinal cord lesion: Evidence of preserved vascular function

A spinal cord injury (SCI) clearly results in greater cardiovascular risk; however, accompanying changes in peripheral vascular structure below the lesion mean that the real impact of a SCI on vascular function is unclear. Aim: Therefore, utilizing passive leg movement-induced (PLM) hyperaemia, an index of nitric oxide (NO)-dependent vascular function and the central hemodynamic response to this intervention, we studied eight individuals with a SCI and eight age-matched controls (CTRL). Methods: Specifically, we assessed heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), leg blood flow (LBF) and thigh composition. Results: In CTRL, passive movement transiently decreased MAP and increased HR and CO from baseline by 2.5 ± 1 mmHg, 7 ± 2 bpm and 0.5 ± 0.1 L min-1 respectively. In SCI, HR and CO responses were unidentifiable. LBF increased to a greater extent in CTRL (515 ± 41 {increment}mL min-1) compared with SCI, (126 ± 25 {increment}mL min-1) (P < 0.05). There was a strong relationship between {increment}LBF and thigh muscle volume (r = 0.95). After normalizing {increment}LBF for this strong relationship ({increment}LBF/muscle volume), there was evidence of preserved vascular function in SCI (CTRL: 120 ± 9; SCI 104 ± 11 mL min-1 L-1). A comparison of {increment}LBF in the passively moved and stationary leg, to partition the contribution of the blood flow response, implied that 35% of the hyperaemia resulted from cardioacceleration in the CTRL, whereas all the hyperaemia appeared peripheral in origin in the SCI. Conclusion: Thus, utilizing PLM-induced hyperaemia as marker of vascular function, it is evident that peripheral vascular impairment is not an obligatory accompaniment to a SCI.