School of Clinical & Experimental Medicine, College of Medical & Dental Sciences, The Medical School, Vincent Drive, University of Birmingham, Birmingham B15 2TT, UK.
J Physiol. 2012 Dec 15;590(24):6307-20. doi: 10.1113/jphysiol.2012.240721. Epub 2012 Oct 8.
This review considers the contributions to exercise hyperaemia of substances released into the interstitial fluid, with emphasis on whether they are endothelium dependent or O(2) dependent. The early phase of exercise hyperaemia is attributable to K(+) released from contracting muscle fibres and acting extraluminally on arterioles. Hyperpolarization of vascular smooth muscle and endothelial cells induced by K(+) may also facilitate the maintained phase, for example by facilitating conduction of dilator signals upstream. ATP is released into the interstitium from muscle fibres, at least in part through cystic fibrosis transmembrane conductance regulator-associated channels, following the fall in intracellular H(+). ATP is metabolized by ectonucleotidases to adenosine, which dilates arterioles via A(2A) receptors, in a nitric oxide-independent manner. Evidence is presented that the rise in arterial achieved by breathing 40% O(2) attenuates efflux of H(+) and lactate, thereby decreasing the contribution that adenosine makes to exercise hyperaemia; efflux of inorganic phosphate and its contribution may likewise be attenuated. Prostaglandins (PGs), PGE(2) and PGI(2), also accumulate in the interstitium during exercise, and breathing 40% O(2) abolished the contribution of PGs to exercise hyperaemia. This suggests that PGE(2) released from muscle fibres and PGI(2) released from capillaries and venular endothelium by a fall in their local act extraluminally to dilate arterioles. Although modest hyperoxia attenuates exercise hyperaemia by improving O(2) supply, limiting the release of O(2)-dependent adenosine and PGs, higher O(2) concentrations may have adverse effects. Evidence is presented that breathing 100% O(2) limits exercise hyperaemia by generating O(2)(-), which inactivates nitric oxide and decreases PG synthesis.
这篇综述考虑了在细胞间液中释放的物质对运动充血的贡献，重点是它们是否依赖于内皮细胞或依赖于 O(2)。运动充血的早期阶段归因于收缩肌纤维释放的 K(+)，并在外周作用于小动脉。K(+)引起的血管平滑肌和内皮细胞的超极化也可能促进维持阶段，例如通过促进上游扩张信号的传导。ATP 至少部分通过囊性纤维化跨膜电导调节体相关通道从肌纤维释放到细胞外间隙，这是由于细胞内 H(+)下降引起的。ATP 被细胞外核苷酸酶代谢为腺苷，通过 A(2A)受体扩张小动脉，这是一种独立于一氧化氮的方式。有证据表明，呼吸 40% O(2)引起的动脉升高减弱了 H(+)和乳酸的流出，从而降低了腺苷对运动充血的贡献；无机磷酸盐的流出及其贡献也可能减弱。前列腺素 (PGs)、PGE(2) 和 PGI(2) 在运动过程中也在细胞外间隙中积累，呼吸 40% O(2) 消除了 PGs 对运动充血的贡献。这表明，从肌纤维释放的 PGE(2)和从毛细血管和小静脉内皮细胞释放的 PGI(2)，通过局部降低其作用于小动脉的能力来扩张小动脉。虽然适度的高氧通过改善 O(2)供应来减弱运动充血，限制了 O(2)依赖性腺苷和 PGs 的释放，但较高的 O(2)浓度可能会产生不良影响。有证据表明，呼吸 100% O(2) 通过产生 O(2)(-)来限制运动充血，O(2)(-)会使一氧化氮失活并减少 PG 合成。
