Krajnak K, Dong R G, Flavahan S, Welcome D, Flavahan N A
National Institute of Occupational Safety and Health, Health Effects Laboratory Division, Engineering and Control Technology Branch, Morgantown, West Virginia, USA.
J Appl Physiol (1985). 2006 Apr;100(4):1230-7. doi: 10.1152/japplphysiol.00761.2005. Epub 2005 Dec 8.
The vascular symptoms of hand-arm vibration syndrome, including cold-induced vasospasm, are in part mediated by increased sensitivity of cutaneous arteries to sympathetic stimulation. The goal of the present study was to use a rat tail model to analyze the effects of vibration on vascular function and alpha-adrenoceptor (AR) responsiveness. Rats were exposed to a single period of vibration (4 h, 125 Hz, constant acceleration 49 m/s2 root mean square). The physical or biodynamic response of the tail demonstrated increased transmissibility or resonance at this frequency, similar to that observed during vibration of human fingers. Morphological analysis demonstrated that vibration did not appear to cause structural injury to vascular cells. In vitro analysis of vascular function demonstrated that constriction to the alpha1-AR agonist phenylephrine was similar in vibrated and control arteries. In contrast, constriction to the alpha2-AR agonist UK14304 was increased in vibrated compared with control arteries, both in endothelium-containing or endothelium-denuded arteries. The alpha2C-AR antagonist MK912 (3 x 10(-10) M) inhibited constriction to UK14304 in vibrated but not control arteries, reversing the vibration-induced increase in alpha2-AR activity. Moderate cooling (to 28 degrees C) increased constriction to the alpha2-AR agonist in control and vibrated arteries, but the magnitude of the amplification was less in vibrated compared with control arteries. Endothelium-dependent relaxation to acetylcholine was similar in control and vibrated arteries. Based on these results, we conclude that a single exposure to vibration caused a persistent increase in alpha2C-AR-mediated vasoconstriction, which may contribute to the pathogenesis of vibration-induced vascular disease.
手臂振动综合征的血管症状，包括冷诱导的血管痉挛，部分是由皮肤动脉对交感神经刺激的敏感性增加介导的。本研究的目的是使用大鼠尾巴模型来分析振动对血管功能和α-肾上腺素能受体（AR）反应性的影响。将大鼠暴露于单个振动周期（4小时，125赫兹，均方根加速度49米/秒²）。尾巴的物理或生物动力学反应表明，在该频率下传递性或共振增加，类似于人类手指振动时观察到的情况。形态学分析表明，振动似乎不会对血管细胞造成结构损伤。血管功能的体外分析表明，振动动脉和对照动脉对α1-AR激动剂去氧肾上腺素的收缩作用相似。相比之下，无论是含内皮还是去内皮的动脉，振动动脉对α2-AR激动剂UK14304的收缩作用都比对照动脉增强。α2C-AR拮抗剂MK912（3×10⁻¹⁰ M）抑制振动动脉对UK14304的收缩作用，但不抑制对照动脉，从而逆转了振动诱导的α2-AR活性增加。适度冷却（至28℃）会增加对照动脉和振动动脉对α2-AR激动剂的收缩作用，但与对照动脉相比，振动动脉的放大幅度较小。对照动脉和振动动脉对乙酰胆碱的内皮依赖性舒张作用相似。基于这些结果，我们得出结论，单次暴露于振动会导致α2C-AR介导的血管收缩持续增加，这可能有助于振动诱导的血管疾病的发病机制。
