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

UNLABELLED: 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.

Human skeletal muscle feed arteries: evidence of regulatory potential.

AIM: Recently, it has been recognized that human skeletal muscle feed arteries can be harvested during exploratory surgery for melanoma. This approach provides vessels for in vitro study from a wide spectrum of relatively healthy humans. Although, the regulatory role of skeletal muscle feed arteries in rodent models has been documented, whether such vessels in humans possess this functionality is unknown. METHODS: Therefore, skeletal muscle feed arteries (~950 µm OD) from 10 humans (48 ± 4, 27-64 years) were studied using pressure myography. Vessel function was assessed using potassium chloride (KCl), phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) concentration-response curves (CRCs) to characterize non-receptor and receptor-mediated vasoconstriction as well as endothelium-dependent and independent vasodilation respectively. To understand the physiological relevance of the diameter changes as a result of pharmacological stimulation, the estimated conductance ratio (CR) was calculated. RESULTS: Vessel function protocols revealed significant vasoconstriction in response to PE and KCl (35 ± 6; 43 ± 9%vasoconstriction, respectively) and significant vasodilation with ACh and SNP (85 ± 7; 121 ± 17% vasodilation, respectively). Both PE and KCl significantly reduced the CR (0.26 ± 0.05 and 0.23 ± 0.07, respectively), whereas ACh and SNP increased the CR (2.56 ± 0.10 and 5.32 ± 1.3, respectively). CONCLUSION: These novel findings provide evidence that human skeletal muscle feed arteries are capable of generating significant diameter changes that would translate into significant changes in vascular conductance. Thus, human skeletal muscle feed arteries likely play a significant role in regulating vascular conductance and subsequently blood flow in vivo.