Energetics in arterioles during nitric oxide dependent and independent vasodilation

本研究的目的是评估一氧化氮（NO）是否会通过降低血管平滑肌的机械功来降低血管壁耗氧量。本文用磷光猝灭法测定了大鼠提睾肌血管内和血管周围氧分压（PO_2），并在此基础上测定了NO依赖性和非依赖性血管舒张时小动脉壁的耗氧率（QO_2）。NO依赖性血管舒张是由于血流量增加导致的NO产生增加而引起的，而NO非依赖性血管舒张是由局部施用罂粟碱引起的。能量效率通过正常和舒张状态下的室壁张力与QO_2的比值来评价。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在两次扩张中均显著降低。NO依赖性和非依赖性舒张血管的能量效率无显著差异，提示NO引起的血管壁QO_2降低与血管平滑肌机械功降低有关。

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.