Just A, Schneider C, Ehmke H, Kirchheim H R
Institut fur Physiologie und Pathophysiologie, Universitat Heidelberg, Im Neuenheimer Feld 326, D-69120 Heidelberg, Germany.
J Physiol. 2000 Sep 15;527 Pt 3(Pt 3):611-22. doi: 10.1111/j.1469-7793.2000.t01-1-00611.x.
Large (up to +400 %) transient ( approximately 20 s) increases of blood flow were observed in the external iliac arteries of resting conscious dogs (n = 10) in the absence of major alerting or muscular activity. At the same time arterial pressure (AP) fell slightly while heart rate (HR) rose. The vasodilatations were resistant to atropine, ganglionic, beta-adrenergic and NO-synthase inhibition, but were suppressed by spinal or general anaesthesia. Vasodilatations of similar appearance were elicited by an alerting sound; these were abolished by atropine. The spontaneous vasodilatations occurred simultaneously and their magnitudes were well correlated between both legs, but were not correlated to the amount of concomitant activation of the surface electromyogram. The duration of this activation almost never outlasted 10 s. The reactive hyperaemia observed after a total occlusion of the artery even for 16 s was not large enough to explain the size of the spontaneous vasodilatations. Occlusion during peak flow of the vasodilatations did not affect the size of the reactive hyperaemia. Spectral analysis made separately for data segments with and without vasodilatation revealed that the vasodilatations substantially enhanced the variability of AP and HR at frequencies below approximately 0.1 Hz. In conclusion, large coordinated skeletal muscle vasodilatations were identified in resting conscious dogs, which are initiated neurally, but not by sympathetic-cholinergic or nitroxidergic fibres and which do not show any clear correlation to muscular contraction. The vasodilatations substantially affect the regulation of skeletal muscle blood flow and explain a significant portion of AP and HR variability.
在无明显警觉或肌肉活动的情况下，观察到10只清醒静息犬的髂外动脉血流出现大幅（高达400%）短暂（约20秒）增加。与此同时，动脉压（AP）略有下降，而心率（HR）上升。这些血管舒张对阿托品、神经节阻断剂、β-肾上腺素能抑制剂和一氧化氮合酶抑制剂均有抵抗作用，但可被脊髓麻醉或全身麻醉所抑制。类似的血管舒张可由警觉声诱发；这些反应可被阿托品消除。自发性血管舒张同时出现，且两条腿的舒张幅度高度相关，但与表面肌电图的伴随激活量无关。这种激活的持续时间几乎从未超过10秒。即使动脉完全闭塞16秒后观察到的反应性充血也不足以解释自发性血管舒张的幅度。在血管舒张的峰值血流期间进行闭塞并不影响反应性充血的大小。对有血管舒张和无血管舒张的数据段分别进行频谱分析表明，血管舒张在频率低于约0.1Hz时显著增强了动脉压和心率的变异性。总之，在清醒静息犬中发现了大量协调性骨骼肌血管舒张，其由神经引发，但不是由交感胆碱能或氮氧化物能纤维引发，且与肌肉收缩无明显相关性。这些血管舒张显著影响骨骼肌血流调节，并解释了动脉压和心率变异性的很大一部分。
