Energetics in arterioles during nitric oxide dependent and independent vasodilation

本研究的目的是评估一氧化氮（NO）是否会通过减少血管平滑肌的机械功来降低血管壁耗氧量。采用磷光猝灭法测定血管内氧张力（PO_2）和血管周围氧张力（PO_2），测定了一氧化氮依赖性和非依赖性血管舒张过程中大鼠肌小动脉壁的耗氧量（QO_2）。一氧化氮依赖性血管舒张是由于血流量增加导致一氧化氮生成增加引起的，而一氧化氮独立性血管舒张是由局部给药罂粟碱引起的。通过血管正常和血管舒张状态下血管壁张力与QO_2的变化率来评价能量效率。NO依赖性和非依赖性扩张分别使小动脉直径增加13%和17%。血管壁QO_2均明显降低。一氧化氮依赖型和非依赖型血管舒张的能量效率差异无统计学意义，提示一氧化氮引起血管壁QO_2的减少可能与血管平滑肌的机械功减少有关。

The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO_2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO_2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO_2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13% and 17%, respectively. Vascular wall QO_2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO_2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.