Wilson Thad E, Cui Jian, Crandall Craig G
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, TX 75231, USA.
Auton Neurosci. 2002 May 31;97(2):122-8. doi: 10.1016/s1566-0702(02)00046-2.
Animal studies suggest that alpha-adrenergic-mediated vasoconstriction is compromised during whole-body heating. The purpose of this study was to identify whether whole-body heating and/or local surface heating reduce cutaneous alpha-adrenergic vasoconstrictor responsiveness in human skin. Protocol I: Six subjects were exposed to neutral skin temperature (i.e., 34 degrees C), whole-body heating, and local heating of forearm skin to increase skin blood flow to the same relative magnitude as that observed during whole-body heating. Protocol II: In eight subjects forearm skin was locally heated to 34, 37, 40, and 42 degrees C. During both protocols, alpha-adrenergic vasoconstrictor responsiveness was assessed by local delivery of norepinephrine (NE) via intradermal microdialysis. Skin blood flow was continuously monitored over each microdialysis membrane via laser-Doppler flowmetry. In protocol I, whole-body and local heating caused similar increases in cutaneous vascular conductance (CVC). The EC50 (log NE dose) of the dose-response curves for both whole body (-4.2 +/- 0.1 M) and local heating (-4.7 +/- 0.4 M) were significantly greater (i.e., high dose required to cause 50% reduction in CVC) relative to neutral skin temperature (- 5.6 +/- 0.0 M; P<0.05 for both). In both local and whole-body heated conditions CVC did not return to pre-heating values even at the highest dose of NE. In protocol II, calculated EC50 for 34, 37, 40, and 42 degrees C local heating was - 5.5 +/- 0.4, -4.6 +/- 0.3, -4.5 +/- 0.3, - 4.2 +/- 0.4 M, respectively. Statistical analyses revealed that the EC50 for 37,40 and 42 degrees C were significantly greater than the EC50 for 34 degrees C. These results indicate that even during administration of high concentrations of NE, alpha-adrenergic vasoconstriction does not fully compensate for local heating and whole-body heating induced vasodilatation in young, healthy subjects. Moreover, these data suggest that elevated local temperatures, above 37 degrees C, and whole-body heating similarly attenuate cutaneous alpha-adrenergic vasoconstriction responsiveness.
动物研究表明,在全身加热过程中,α-肾上腺素能介导的血管收缩作用会受到损害。本研究的目的是确定全身加热和/或局部表面加热是否会降低人体皮肤中α-肾上腺素能血管收缩反应性。方案一:六名受试者分别暴露于中性皮肤温度(即34摄氏度)、全身加热以及前臂皮肤局部加热环境中,以使皮肤血流量增加至与全身加热时观察到的相对幅度相同。方案二:八名受试者的前臂皮肤被局部加热至34、37、40和42摄氏度。在两个方案实施过程中,通过皮内微透析局部给予去甲肾上腺素(NE)来评估α-肾上腺素能血管收缩反应性。通过激光多普勒血流仪在每个微透析膜上持续监测皮肤血流量。在方案一中,全身加热和局部加热导致皮肤血管传导性(CVC)出现类似增加。全身加热(-4.2±0.1M)和局部加热(-4.7±0.4M)时剂量-反应曲线的半数有效浓度(EC50,log NE剂量)相对于中性皮肤温度(-5.6±0.0M)均显著更高(即导致CVC降低50%所需的高剂量)(两者P<0.05)。在局部和全身加热条件下,即使给予最高剂量的NE,CVC也未恢复到加热前的值。在方案二中,34、37、40和42摄氏度局部加热时计算出的EC50分别为-5.5±0.4、-4.6±0.3、-4.5±0.3、-4.2±0.4M。统计分析显示,37、40和42摄氏度时的EC50显著高于34摄氏度时的EC50。这些结果表明,即使在给予高浓度NE的情况下,α-肾上腺素能血管收缩也不能完全补偿年轻健康受试者中局部加热和全身加热引起的血管舒张。此外,这些数据表明,高于37摄氏度的局部温度升高和全身加热同样会减弱皮肤α-肾上腺素能血管收缩反应性。