Pál M, Tóth A, Ping P, Johnson P C
Department of Physiology, University of Arizona College of Medicine, Tucson 85724, USA.
Am J Physiol. 1998 Feb;274(2):H430-40. doi: 10.1152/ajpheart.1998.274.2.H430.
NADH fluorescence at tissue sites 15-20 microns in diameter and red blood cell velocity in adjacent capillaries were measured in resting sartorius muscle of the anesthetized cat during a 3-min period of sympathetic trunk stimulation. At stimulation frequencies of 2 and 4 Hz, red blood cell velocity fell briefly to 30-40% of control and then returned to approximately 75% of control values (vascular escape). No change in NADH fluorescence was observed. With stimulus frequencies of 6-12 Hz, flow reduction was greater and led to an increase in fluorescence when the flow reduction was > 50% and was sustained for > 30 s. NADH changes were more pronounced at tissue sites near venous capillaries than at sites near arterial capillaries. Hyperemia ensued after the end of sympathetic stimulation only when NADH fluorescence rose during stimulation. Resting blood flow in this muscle appears to be well above the minimum required to support oxidative metabolism. A shift to anaerobic metabolism does not appear to cause vascular escape during sympathetic stimulation but appears to be required for poststimulation hyperemia. These observations suggest that two separate oxygen-dependent mechanisms elicit vasodilation during and after sympathetic trunk stimulation.
在对麻醉猫的缝匠肌进行3分钟交感干刺激期间，测量了直径15 - 20微米的组织部位的NADH荧光以及相邻毛细血管中的红细胞速度。在2赫兹和4赫兹的刺激频率下，红细胞速度短暂降至对照值的30% - 40%，然后恢复到对照值的约75%（血管逃逸）。未观察到NADH荧光有变化。在6 - 12赫兹的刺激频率下，血流减少幅度更大，当血流减少>50%并持续>30秒时，会导致荧光增加。NADH的变化在静脉毛细血管附近的组织部位比在动脉毛细血管附近的部位更明显。仅当刺激期间NADH荧光升高时，交感刺激结束后才会出现充血。该肌肉的静息血流似乎远高于支持氧化代谢所需的最小值。在交感刺激期间，向无氧代谢的转变似乎不会导致血管逃逸，但似乎是刺激后充血所必需的。这些观察结果表明，在交感干刺激期间和之后，有两种独立的氧依赖机制引发血管舒张。
