Passive leg movement (PLM) evokes a robust and predominantly nitric oxide (NO)-mediated increase in blood flow that declines with age and disease. Consequently, PLM is becoming increasingly accepted as a sensitive assessment of endothelium-mediated vascular function. However, a substantial PLM-induced hyperemic response is still evoked despite NO synthase (NOS) inhibition. Therefore, in 9 young healthy men (25±4 yrs), this investigation aimed to determine if the combination of two potent endothelium-dependent vasodilators, specifically prostaglandin (PG) and endothelium-derived hyperpolarizing factor (EDHF), account for the remaining hyperemic response to the two variants of PLM, PLM (60 movements) and single PLM (sPLM, 1 movement) when NOS is inhibited. The leg blood flow (LBF, Doppler ultrasound) response to PLM and sPLM following the intra-arterial infusion of N^G-monomethyl _L-arginine (L-NMMA), to inhibit NOS, was compared to the combined inhibition of NOS, cyclooxygenase (COX), and cytochrome P450 (CYP450) by L-NMMA, ketorolac tromethamine (KET), and fluconazole (FLUC), respectively. NOS inhibition attenuated the overall LBF (LBF_AUC) response to both PLM (control: 456±194, L-NMMA: 168±127 ml, p<0.01) and sPLM(control: 185±171, L-NMMA: 62±31 ml, p=0.03). The combined inhibition of NOS, COX, and CYP450 (i.e. L-NMMA+KET+FLUC) did not further attenuate the hyperemic responses to PLM (LBF_AUC: 271±97 ml, p>0.05) or sPLM (LBF_AUC: 72±45 ml, p>0.05). Therefore, PG and EDHF do not collectively contribute to the non-NOS-derived NO-mediated, endothelium-dependent, hyperemic response to either PLM or sPLM in healthy young men. These findings add to the mounting evidence and understanding of the vasodilatory pathways assessed by the PLM and sPLM vascular function tests.

中文翻译：

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内皮在对被动腿部运动的充血反应中的作用：超越一氧化氮

被动腿部运动 (PLM) 会引起强烈且主要由一氧化氮 (NO) 介导的血流量增加，这种增加会随着年龄和疾病而下降。因此，PLM 越来越被接受为内皮介导的血管功能的敏感评估。然而，尽管 NO 合酶 (NOS) 受到抑制，但仍会引发大量 PLM 诱导的充血反应。因此，在 9 名年轻的健康男性（25±4 岁）中，本研究旨在确定两种有效的内皮依赖性血管扩张剂，特别是前列腺素 (PG) 和内皮源性超极化因子 (EDHF) 的组合是否解释了剩余的充血当 NOS 被抑制时，对 PLM 的两种变体，PLM（60 次运动）和单个 PLM（sPLM，1 次运动）的响应。腿部血流（LBF，^{将抑制 NOS 的G-}单甲基_L-精氨酸 (L-NMMA) 与 L-NMMA、酮咯酸氨丁三醇 (KET) 和氟康唑联合抑制 NOS、环氧合酶 (COX) 和细胞色素 P450 (CYP450) 进行比较。 FLUC），分别。NOS 抑制减弱了对 PLM（对照：456±194，L-NMMA：168±127 ml，p<0.01）和 sPLM 的总体 LBF (LBF _AUC ) 反应（对照：185±171，L-NMMA：62±31 ml，p=0.03）。NOS、COX 和 CYP450 的联合抑制（即 L-NMMA+KET+FLUC）并未进一步减弱对 PLM（LBF _AUC：271±97 ml，p>0.05）或 sPLM（LBF _AUC：72± ）的充血反应45 毫升，p > 0.05)。因此，PG 和 EDHF 不会共同促成健康年轻男性对 PLM 或 sPLM 的非 NOS 衍生的 NO 介导的、内皮依赖性的充血反应。这些发现增加了对 PLM 和 sPLM 血管功能测试评估的血管扩张途径的越来越多的证据和理解。