Wang H X, Davis M J, Rajanayagam M A, Potocnik S J, Hill M A
Microvascular Biology Group, Department of Human Biology and Movement Science, RMIT University, Bundoora, Victoria 3083, Australia.
Am J Physiol. 1999 Jul;277(1):H144-51. doi: 10.1152/ajpheart.1999.277.1.H144.
Local control of neural blood flow is considered to reside in innervation of epineurial and endoneurial arterioles rather than in intrinsic autoregulatory mechanisms. With the use of an isolated vessel preparation and an in vivo approach, the present studies examined intrinsic vasomotor responsiveness of epineurial arterioles. Segments of epineurial arterioles, cannulated on glass micropipettes (40 micrometers) and pressurized in the absence of intraluminal flow, showed sustained pressure-dependent (30-90 mmHg) vasoconstriction and acute myogenic reactivity. Myogenic tone was unaffected by phentolamine (10(-6) M). Removal of extracellular Ca(2+) resulted in loss of spontaneous tone and passive behavior. Concentration-response curves for norepinephrine (10(-9)-3 x 10(-6) M) and relaxation to both acetylcholine (10(-8)-10(-5) M) and adenosine (10(-8)-10(-4) M) were obtained. Acetylcholine dilator responses were inhibited by N(G)-nitro-L-arginine methyl ester. Epineurial blood flow was measured in vivo using a laser-Doppler flow probe. Blood flow declined over a 2-h period after surgery, and during this time preparations developed responsiveness to the dilator acetylcholine. Phentolamine blocked vasoconstrictor responses to exogenous norepinephrine but only partially reversed the in vivo baseline tone. The time-dependent decline in epineurial blood flow was observed despite the presence of tetrodotoxin (1 microM), further confirming that tone was predominantly caused by myogenic rather than neurogenic mechanisms. It is concluded that because epineurial arterioles exhibit intrinsic myogenic reactivity, they have the potential to participate in local regulation of neural hemodynamics independently of their own innervation.
神经血流的局部控制被认为存在于神经外膜和神经内膜小动脉的神经支配中，而非内在的自身调节机制。通过使用离体血管制备和体内研究方法，本研究检测了神经外膜小动脉的内在血管舒缩反应性。将神经外膜小动脉段插管于玻璃微吸管（40微米）上，并在无腔内血流的情况下加压，结果显示出持续的压力依赖性（30 - 90 mmHg）血管收缩和急性肌源性反应性。肌源性张力不受酚妥拉明（10⁻⁶ M）影响。去除细胞外Ca²⁺导致自发张力丧失和被动行为。获得了去甲肾上腺素（10⁻⁹ - 3×10⁻⁶ M）的浓度 - 反应曲线以及对乙酰胆碱（10⁻⁸ - 10⁻⁵ M）和腺苷（10⁻⁸ - 10⁻⁴ M）的舒张反应曲线。N⁰ - 硝基 - L - 精氨酸甲酯抑制了乙酰胆碱的舒张反应。使用激光多普勒血流探头在体内测量神经外膜血流。术后2小时内血流下降，在此期间制备物对舒张剂乙酰胆碱产生反应性。酚妥拉明阻断了对外源性去甲肾上腺素的血管收缩反应，但仅部分逆转了体内基线张力。尽管存在河豚毒素（1 microM），仍观察到神经外膜血流随时间下降，进一步证实张力主要由肌源性而非神经源性机制引起。得出的结论是，由于神经外膜小动脉表现出内在的肌源性反应性，它们有可能独立于自身神经支配参与神经血流动力学的局部调节。
