Crandall C G, Shibasaki M, Yen T C
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, TX 75231, USA.
J Physiol. 2002 Jan 15;538(Pt 2):599-605. doi: 10.1113/jphysiol.2001.013060.
The venoarteriolar response causes vasoconstriction to skin and muscle via local mechanisms secondary to venous congestion. The purpose of this project was to investigate whether this response occurs through alpha-adrenergic mechanisms. In supine individuals, forearm skin blood flow was monitored via laser-Doppler flowmetry over sites following local administration of terazosin (alpha(1)-antagonist), yohimbine (alpha(2)-antagonist), phentolamine (non-selective alpha-antagonist) and bretylium tosylate (inhibits neurotransmission of adrenergic nerves) via intradermal microdialysis or intradermal injection. In addition, skin blood flow was monitored over an area of forearm skin that was locally anaesthetized via application of EMLA (2.5 % lidocaine (lignocaine) and 2.5 % prilocaine) cream. Skin blood flow was also monitored over adjacent sites that received the vehicle for the specified drug. Each trial was performed on a minimum of seven subjects and on separate days. The venoarteriolar response was engaged by lowering the subject's arm from heart level such that the sites of skin blood flow measurement were 34 +/- 1 cm below the heart. The arm remained in this position for 2 min. Selective and non-selective alpha-adrenoceptor antagonism and presynaptic inhibition of adrenergic neurotransmission did not abolish the venoarteriolar response. However, local anaesthesia blocked the venoarteriolar response without altering alpha-adrenergic mediated vasoconstriction. These data suggest that the venoarteriolar response does not occur through adrenergic mechanisms as previously reported. Rather, the venoarteriolar response may due to myogenic mechanisms associated with changes in vascular pressure or is mediated by a non-adrenergic, but neurally mediated, local mechanism.
静脉小动脉反应通过静脉充血继发的局部机制导致皮肤和肌肉血管收缩。本项目的目的是研究这种反应是否通过α-肾上腺素能机制发生。在仰卧位个体中，通过激光多普勒血流仪监测前臂皮肤血流量，监测部位为经皮内微透析或皮内注射给予特拉唑嗪（α₁拮抗剂）、育亨宾（α₂拮抗剂）、酚妥拉明（非选择性α拮抗剂）和甲苯磺酸溴苄铵（抑制肾上腺素能神经的神经传递）后的部位。此外，通过涂抹EMLA（2.5%利多卡因和2.5%丙胺卡因）乳膏对前臂皮肤局部麻醉区域的皮肤血流量进行监测。还对接受特定药物载体的相邻部位的皮肤血流量进行了监测。每个试验至少在7名受试者身上进行，且在不同日期进行。通过将受试者的手臂从心脏水平放下，使皮肤血流量测量部位位于心脏下方34±1厘米，从而引发静脉小动脉反应。手臂保持在这个位置2分钟。选择性和非选择性α-肾上腺素能受体拮抗以及肾上腺素能神经传递的突触前抑制并未消除静脉小动脉反应。然而，局部麻醉阻断了静脉小动脉反应，而未改变α-肾上腺素能介导的血管收缩。这些数据表明，静脉小动脉反应并非如先前报道的那样通过肾上腺素能机制发生。相反，静脉小动脉反应可能归因于与血管压力变化相关的肌源性机制，或者是由一种非肾上腺素能但由神经介导的局部机制介导。
