VanTeeffelen Jurgen W G E, Segal Steven S
The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06519, USA.
J Physiol. 2003 Jul 15;550(Pt 2):563-74. doi: 10.1113/jphysiol.2003.038984. Epub 2003 May 16.
The interaction between skeletal muscle contraction and sympathetic nerve activation (SNA) on blood flow during exercise has remained ambiguous due to indirect estimates of vasomotor control. In the hamster retractor muscle (n=54), interactions between three levels of SNA (approximately 3, 6 and 12 Hz) and of contractile activity (2.5, 10 and 20 % duty cycle) were studied in feed arteries (FA) and first- (1A), second- (2A), and third-order (3A) arterioles using intravital microscopy. During functional dilatation with rhythmic muscle contractions, sympathetic vasoconstriction was sustained in FA and 1A but impaired in 2A and 3A (P<0.05), where vessels 'escaped' from responding to SNA. To account for changes in baseline diameter and blood flow during contractions, vasodilatation was induced passively (2-3 levels) in resting muscles with papaverine or sodium nitroprusside. Compared to functional dilatation, the range of passive dilatation was similar in 3A and progressively greater in 2A, 1A and FA. With passive dilatation, SNA responses were sustained in 2A and increased with baseline diameter in 3A. Blood flow through FA (rest, approximately 20 nl s(-1)) increased approximately 5-fold during contractile activity and approximately 10-fold during passive dilatation. Absolute flow reductions (nl s(-1)) with SNA increased during contractile activity and during passive dilatation; relative flow reductions were impaired during functional dilatation (P<0.05) and remained constant during passive dilatation. Thus, SNA can restrict blood flow to exercising muscle by constricting FA and 1A while dilatation prevails in 2A and 3A. Such concerted interaction will promote oxygen extraction when blood flow is restricted to maintain arterial pressure.
由于对血管舒缩控制的间接估计，运动期间骨骼肌收缩与交感神经激活（SNA）对血流的相互作用一直不明确。在仓鼠牵张肌（n = 54）中，使用活体显微镜研究了三个SNA水平（约3、6和12 Hz）与收缩活动（2.5%、10%和20%占空比）在供血动脉（FA）以及一级（1A）、二级（2A）和三级（3A）小动脉中的相互作用。在有节律性肌肉收缩引起的功能性扩张期间，FA和1A中的交感神经血管收缩得以维持，但在2A和3A中受损（P<0.05），在2A和3A中血管“逃脱”了对SNA的反应。为了解释收缩期间基线直径和血流的变化，在静息肌肉中用罂粟碱或硝普钠被动诱导血管舒张（2 - 3个水平）。与功能性扩张相比，3A中被动扩张的范围相似，而在2A、1A和FA中逐渐增大。在被动扩张时，2A中SNA反应得以维持，3A中SNA反应随基线直径增加。通过FA的血流（静息时约20 nl s⁻¹）在收缩活动期间增加约5倍，在被动扩张期间增加约10倍。随着SNA的绝对血流减少量（nl s⁻¹）在收缩活动期间和被动扩张期间均增加；功能性扩张期间相对血流减少受损（P<0.05），被动扩张期间相对血流减少保持恒定。因此，SNA可通过收缩FA和1A来限制流向运动肌肉的血流，而2A和3A则以扩张为主。当血流受限以维持动脉压时，这种协同相互作用将促进氧气摄取。
