Πέμπτη 31 Αυγούστου 2017

Single passive leg movement assessment of vascular function: The contribution of nitric oxide

The assessment of passive leg movement (PLM)-induced leg blood flow (LBF) and vascular conductance (LVC) is a novel approach to assess vascular function, which has recently been simplified to only a single PLM (sPLM), thereby increasing the clinical utility of this technique. As the physiological mechanisms mediating the robust increase in LBF and LVC with sPLM are currently unknown, we tested the hypothesis that nitric oxide (NO) is a major contributor to the sPLM-induced LBF and LVC response. In nine healthy men, sPLM was performed with and without the inhibition of nitric oxide synthase (NOS) via intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA). Doppler ultrasound and femoral arterial pressure were used to determine LBF and LVC, which were characterized by the peak change (LBFpeak and LVCpeak) and area under the curve (LBFAUC and LVCAUC). L-NMMA significantly attenuated the LBFpeak (L-NMMA: 492 ± 153 vs. control: 719 ± 238 ml·min-1), LBFAUC (L-NMMA: 57 ± 34 vs. control: 147 ± 63 ml), LVCpeak (L-NMMA: 4.7 ± 1.1 vs. control: 8.0 ± 3.0 ml·min-1·mmHg-1), and the LVCAUC (L-NMMA: 0.5 ± 0.3 vs. control: 1.6 ± 0.9 ml·mmHg-1). The magnitude of NO contribution to LBF and LVC was significantly correlated with the magnitude of the control responses (LBFpeak: r = 0.94; LBFAUC: r = 0.85; LVCpeak: r = 0.94; LVCAUC: r = 0.95). These data establish that the sPLM-induced hyperemic and vasodilatory response is predominantly (~65%) NO-mediated. As such, sPLM appears to be a promising, simple, in vivo assessment of NO-mediated vascular function and NO bioavailability.



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