Passive leg movement-induced hyperaemia with a spinal cord lesion: evidence of preserved vascular function

Abstract

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 ∆mL min(-1)) compared with SCI, (126 ± 25 ∆mL min(-1)) (P < 0.05). There was a strong relationship between ∆LBF and thigh muscle volume (r = 0.95). After normalizing ∆LBF for this strong relationship (∆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 ∆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.

Keywords: blood flow; spinal cord injury; vascular dysfunction.

© 2013 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

Figures

Figure 1. Hyperemic response to passive limb movement (PLM) in subjects with a spinal cord injury (SCI) and able-bodied controls (CTRL)

Data are mean ± SEM; * significantly different from baseline in the CTRL; § significantly different from baseline in SCI group; and gray area indicates significantly lower values in the SCI group compared to CTRL.

Figure 2. Evidence of the impact of a spinal cord injury (SCI) on thigh muscle volume (Panel A), the strong link between thigh muscle volume and passive limb movement (PLM)-induced hyperemia (Panel B), and PLM-induced hyperemia normalized for muscle volume in subjects SCI and able-bodied controls (CTRL)

Panel A: 3 mid-thigh magnetic resonance images of a CTRL (I) and 2 subjects with a complete SCI 6 (II) and 16 yrs (II) after the injury. Panel B: Significant correlation between changes in blood flow and thigh muscle volume in SCI, (r = 0.95; p

Figure 3. HR, SV, CO and MAP responses to passive limb movement (PLM) in subjects with a spinal cord injury (SCI) and able-bodied controls (CTRL)

Panels A, B, C, and D illustrate mean arterial pressure (MAP), stroke volume (SV), heart rate (HR), and cardiac output (CO) over time, respectively. Data are mean ± SEM; * significantly different from baseline in the CTRL group.

Figure 4. Partitioning the central and peripheral contributors to passive leg movement (PLM)-induced hyperemia in subjects with a spinal cord injury (SCI) and able-bodied controls (CTRL)

Panels A, and B illustrate leg blood flow in the control leg, and the difference between leg blood flow in the passive and control legs, respectively. Panel C illustrates the % contribution of central and peripheral factors based upon these assessments. Data in Panels A, and B are mean ± SEM; * significantly different from baseline in the CTRL, § significantly different from baseline in SCI group, and gray area in Panel A indicates significantly lower values in the SCI group compared to CTRL.

Figure 5. Schematic illustration of the differing responses to passive leg movement (PLM) in subjects with a spinal cord injury (SCI) and able-bodied controls (CTRL)

In CTRL, neurological feedback from the moving limb triggers central responses (increasing HR and CO) which results in an increase in leg blood flow in the non-moving leg (CONTROL LEG) and the moving leg (PASSIVE LEG), accounting for ~35% of the increase in leg blood flow in the latter. Peripheral vasodilation is responsible for the remaining ~65% increase in leg blood flow in the PASSIVE LEG. In contrast, in the SCI group, there is no feedback from the passively moved limb and so there is no increase in HR and CO, which can contribute to raising blood flow in the CONTROL LEG and the PASSIVE LEG. Hence, in subjects with a SCI, peripheral vasodilation is responsible for all the movement-induced increase in leg blood flow in the PASSIVE LEG.