Widegren U, Hickner R C, Jorfeldt L, Henriksson J
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Clin Physiol Funct Imaging. 2010 Mar;30(2):152-61. doi: 10.1111/j.1475-097X.2009.00919.x. Epub 2010 Jan 26.
Adrenaline, administered locally by microdialysis in skeletal muscle, causes vasoconstriction around the microdialysis catheter. This is contrary to the vasodilation that normally occurs when adrenaline is infused intravenously or intra-arterially. The hypothesis was tested that vasoconstriction, measured by microdialysis, would not occur with two interventions causing increased plasma levels of adrenaline, mental stress and intravenous adrenaline infusion (0.1 nmol kg(-1) min(-1)).
Twenty-four men (27 +/- 1.6 years) underwent these interventions. Blood flow was determined by the microdialysis ethanol technique and (133)Xe clearance (gastrocnemius muscle, medial head) and by venous occlusion plethysmography (calf).
The ethanol outflow/inflow ratio, which is inversely related to blood flow, decreased to 92.0 +/- 3.4% of basal, P = 0.014 (mean +/- SEM, n = 16) during the mental stress test, but increased to 108.3 +/- 2.2% of basal, P = 0.001 (n = 16) during the adrenaline infusion. The latter increase was abolished when adrenaline was infused during alpha-receptor blockade by phentolamine. On the contrary, by (133)Xe clearance and venous occlusion plethysmography, blood flow increased during both interventions; 2.0-1.7-fold (mental stress) and 1.3-1.4-fold (adrenaline infusion), respectively, P<0.05.
Adrenaline causes vasoconstriction in skeletal muscle when blood flow is measured with the microdialysis ethanol technique, irrespective of the mode of administration. The discrepant blood flow result obtained with the microdialysis ethanol technique might, at least partly, be explained by differential diffusion properties of ethanol and (133)Xe. An additional or alternative explanation might be that an inserted microdialysis catheter shifts the balance of vasoconstrictor and vasodilator effects of adrenaline in skeletal muscle.
通过微透析局部给予骨骼肌肾上腺素会导致微透析导管周围血管收缩。这与静脉内或动脉内注射肾上腺素时通常发生的血管舒张相反。本研究对以下假设进行了验证：通过微透析测量，在两种导致血浆肾上腺素水平升高的干预措施（精神应激和静脉注射肾上腺素（0.1 nmol·kg⁻¹·min⁻¹））下不会发生血管收缩。
24名男性（27±1.6岁）接受了这些干预措施。采用微透析乙醇技术和（133）Xe清除法（腓肠肌内侧头）以及静脉阻断体积描记法（小腿）测定血流量。
与血流量呈负相关的乙醇流出/流入比在精神应激测试期间降至基础值的92.0±3.4%，P = 0.014（平均值±标准误，n = 16），但在肾上腺素输注期间升至基础值的108.3±2.2%，P = 0.001（n = 16）。当在酚妥拉明α受体阻断期间输注肾上腺素时，后一种升高被消除。相反，通过（133）Xe清除法和静脉阻断体积描记法，在两种干预措施期间血流量均增加；分别增加2.0 - 1.7倍（精神应激）和1.3 - 1.4倍（肾上腺素输注），P<0.05。
无论给药方式如何，当用微透析乙醇技术测量血流量时，肾上腺素会导致骨骼肌血管收缩。微透析乙醇技术获得的血流量差异结果可能至少部分是由乙醇和（133）Xe的不同扩散特性所解释。另一种或替代的解释可能是，插入的微透析导管改变了骨骼肌中肾上腺素血管收缩和血管舒张作用的平衡。
