Haug Sara J, Welsh Donald G, Segal Steven S
The John B. Pierce Laboratory, Department of Cellular and Molecular Physiology, Yale University, 290 Congress Avenue, New Haven, CT 06519, USA.
J Physiol. 2003 Oct 1;552(Pt 1):273-82. doi: 10.1113/jphysiol.2003.046284. Epub 2003 Aug 1.
Ascending vasodilatation is integral to blood flow control in exercising skeletal muscle and is attributable to conduction from intramuscular arterioles into proximal feed arteries. Passive stretch of skeletal muscle can impair muscle blood flow but the mechanism is not well understood. We hypothesized that the conduction of vasodilatation along feed arteries can be modulated by changes in muscle length. In anaesthetized hamsters, acetylcholine (ACh) microiontophoresis triggered conducted vasodilatation along feed arteries (diameter, 50-70 microm) of the retractor muscle secured at 100 % resting length or stretched by 30 %. At 100 % length, ACh evoked local dilatation (> 30 microm) and this response conducted rapidly along the feed artery (14 +/- 1 microm dilatation at 1600 microm upstream). During muscle stretch, feed arteries constricted approximately 10 microm (P < 0.05) and local vasodilatation to ACh was maintained while conducted vasodilatation was reduced by half (P < 0.01). Resting diameter and conduction recovered upon restoring 100 % length. Sympathetic nerve stimulation (4-8 Hz) produced vasoconstriction and attenuated conduction in the manner observed during muscle stretch, as did noradrenaline or phenylephrine (10 nM). Inhibiting nitric oxide production (Nomega-nitro-L-arginine, 50 microM) produced similar vasoconstriction yet had no effect on conduction. Phentolamine, prazosin, or tetrodotoxin (1 microM) during muscle stretch abolished vasoconstriction and restored conduction. Inactivation of sensory nerves with capsaicin had no effect on vasomotor responses. Thus, muscle stretch can attenuate conducted vasodilatation by activating alpha-adrenoreceptors on feed arteries through noradrenaline released from perivascular sympathetic nerves. This autonomic feedback mechanism can restrict muscle blood flow during passive stretch.
在运动的骨骼肌中，血管舒张的上行传导对于血流控制至关重要，这归因于从肌内小动脉向近端供血动脉的传导。骨骼肌的被动拉伸会损害肌肉血流，但其机制尚不清楚。我们推测，沿供血动脉的血管舒张传导可受肌肉长度变化的调节。在麻醉的仓鼠中，乙酰胆碱（ACh）微离子电渗法引发沿固定于静息长度100%或拉伸30%的牵开肌供血动脉（直径50 - 70微米）的传导性血管舒张。在100%长度时，ACh引起局部扩张（> 30微米），此反应沿供血动脉迅速传导（上游1600微米处扩张14±1微米）。在肌肉拉伸过程中，供血动脉收缩约10微米（P < 0.05），对ACh的局部血管舒张得以维持，而传导性血管舒张减少一半（P < 0.01）。恢复到100%长度后，静息直径和传导恢复。交感神经刺激（4 - 8赫兹）产生血管收缩并以肌肉拉伸时观察到的方式减弱传导，去甲肾上腺素或苯肾上腺素（10纳摩尔）也有同样效果。抑制一氧化氮生成（Nω-硝基-L-精氨酸，50微摩尔）产生类似的血管收缩，但对传导无影响。在肌肉拉伸过程中，酚妥拉明、哌唑嗪或河豚毒素（1微摩尔）消除血管收缩并恢复传导。用辣椒素使感觉神经失活对血管舒缩反应无影响。因此，肌肉拉伸可通过血管周围交感神经释放的去甲肾上腺素激活供血动脉上的α-肾上腺素能受体来减弱传导性血管舒张。这种自主反馈机制可在被动拉伸期间限制肌肉血流。
