Passive leg movement‐induced hyperaemia 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 the real impact of a SCI on vascular function is unclear. Therefore, utilizing passive leg movement-induced (PLM) hyperemia, an index of nitric oxide (NO)-dependent vascular function, and the central hemodynamic response to this intervention, we studied 8 individuals with a SCI, and 8 age-matched controls (CTRL). Specifically, we assessed heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), leg blood flow (LBF), and thigh composition. 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 respectively. In SCI, HR and CO responses were unidentifiable. LBF increased to a greater extent in CTRL (515±41 Δml/min) compared to SCI, (126±25 Δml/min) (p<0.05). There was a strong relationship between ΔLBF and thigh muscle volume (r = 0.95). After normalizing ΔLBF for this strong relationship (ΔLBF/muscle volume), there was evidence of preserved vascular function in SCI (CTRL: 120±9; SCI 104±11 ml/min/l). A comparison of ΔLBF in the passively moved and stationary leg, to partition the contribution of the blood flow response, implied that 35% of the hyperemia resulted from cardioacceleration in the CTRL, whereas all the hyperemia appeared peripheral in origin in the SCI. Thus, utilizing PLM-induced hyperemia as marker of vascular function, it is evident that peripheral vascular impairment is not an obligatory accompaniment to a SCI.