Holowatz Lacy A, Houghton Belinda L, Wong Brett J, Wilkins Brad W, Harding Aaron W, Kenney W Larry, Minson Christopher T
Department of Exercise and Movement Science, University of Oregon, Eugene, OR 97403-1240, USA.
Am J Physiol Heart Circ Physiol. 2003 May;284(5):H1662-7. doi: 10.1152/ajpheart.00871.2002. Epub 2002 Dec 27.
Thermoregulatory cutaneous vasodilation is diminished in the elderly. The goal of this study was to test the hypothesis that a reduction in nitric oxide (NO)-dependent mechanisms contributes to the attenuated reflex cutaneous vasodilation in older subjects. Seven young (23 +/- 2 yr) and seven older (71 +/- 6 yr) men were instrumented with two microdialysis fibers in the forearm skin. One site served as control (Ringer infusion), and the second site was perfused with 10 mM N(G)-nitro-l-arginine methyl ester to inhibit NO synthase (NOS) throughout the protocol. Water-perfused suits were used to raise core temperature 1.0 degrees C. Red blood cell (RBC) flux was measured with laser-Doppler flowmetry over each microdialysis fiber. Cutaneous vascular conductance (CVC) was calculated as RBC flux per mean arterial pressure, with values expressed as a percentage of maximal vasodilation (infusion of 28 mM sodium nitroprusside). NOS inhibition reduced CVC from 75 +/- 6% maximal CVC (CVC(max)) to 53 +/- 3% CVC(max) in the young subjects and from 64 +/- 5% CVC(max) to 29 +/- 2% CVC(max) in the older subjects with a 1.0 degrees C rise in core temperature. Thus the relative NO-dependent portion of cutaneous active vasodilation (AVD) accounted for approximately 23% of vasodilation in the young subjects and 60% of the vasodilation in the older subjects at this level of hyperthermia (P < 0.001). In summary, NO-mediated pathways contributed more to the total vasodilatory response of the older subjects at high core temperatures. This suggests that attenuated cutaneous vasodilation with age may be due to a reduction in, or decreased vascular responsiveness to, the unknown neurotransmitter(s) mediating AVD.
老年人的体温调节性皮肤血管舒张功能减弱。本研究的目的是检验以下假设：一氧化氮（NO）依赖性机制的降低导致老年受试者反射性皮肤血管舒张减弱。七名年轻男性（23±2岁）和七名老年男性（71±6岁）在前臂皮肤植入两根微透析纤维。一个部位作为对照（林格氏液灌注），另一个部位在整个实验过程中灌注10 mM N(G)-硝基-L-精氨酸甲酯以抑制一氧化氮合酶（NOS）。使用水灌注服将核心体温升高1.0℃。通过激光多普勒血流仪测量每根微透析纤维上的红细胞（RBC）流量。皮肤血管传导率（CVC）计算为RBC流量除以平均动脉压，其值表示为最大血管舒张（灌注28 mM硝普钠）的百分比。在年轻受试者中，核心体温升高1.0℃时，NOS抑制使CVC从最大CVC（CVC(max)）的75±6%降至53±3% CVC(max)；在老年受试者中，从64±5% CVC(max)降至29±2% CVC(max)。因此，在该热应激水平下，皮肤主动血管舒张（AVD）中相对NO依赖性部分在年轻受试者的血管舒张中约占23%，在老年受试者的血管舒张中约占60%（P<0.001）。总之，在高核心体温时NO介导的途径对老年受试者的总血管舒张反应贡献更大。这表明随着年龄增长皮肤血管舒张减弱可能是由于介导AVD的未知神经递质减少或血管对其反应性降低所致。
