Wilkins Brad W, Martin Elizabeth A, Roberts Shelly K, Joyner Michael J
Department of Anesthesiology, Mayo Clinic, 200 First St. SW., Rochester, MN 55905, USA.
J Appl Physiol (1985). 2007 Jun;102(6):2301-6. doi: 10.1152/japplphysiol.00013.2007. Epub 2007 Apr 5.
In humans, vasoactive intestinal peptide (VIP) may play a role in reflex cutaneous vasodilation during body heating. We tested the hypothesis that the nitric oxide (NO)-dependent contribution to active vasodilation is enhanced in the skin of subjects with cystic fibrosis (CF), compensating for sparse levels of VIP. In 2 parallel protocols, microdialysis fibers were placed in the skin of 11 subjects with CF and 12 controls. Lactated Ringer was perfused at one microdialysis site and NG-nitro-L-arginine methyl ester (2.7 mg/ml) was perfused at a second microdialysis site. Skin blood flow was monitored over each site with laser-Doppler flowmetry. In protocol 1, local skin temperature was increased 0.5 degrees C every 5 s to 42 degrees C, and then it maintained at 42 degrees C for approximately 45 min. In protocol 2, subjects wore a tube-lined suit perfused with water at 50 degrees C, sufficient to increase oral temperature (Tor) 0.8 degrees C. Cutaneous vascular conductance (CVC) was calculated (flux/mean arterial pressure) and scaled as percent maximal CVC (sodium nitroprusside; 8.3 mg/ml). Vasodilation to local heating was similar between groups. The change (Delta%CVCmax) in CVC with NO synthase inhibition on the peak (9+/-3 vs. 12+/-5%CVCmax; P=0.6) and the plateau (45+/-3 vs. 35+/-5%CVCmax; P=0.1) phase of the skin blood flow response to local heating was similar in CF subjects and controls, respectively. Reflex cutaneous vasodilation increased CVC in CF subjects (58+/-4%CVCmax) and controls (53+/-4%CVCmax; P=0.37) and NO synthase inhibition attenuated CVC in subjects with CF (37+/-6%CVCmax) and controls (35+/-5%CVCmax; P=0.8) to a similar degree. Thus the preservation of cutaneous active vasodilation in subjects with CF is not associated with an enhanced NO-dependent vasodilation.
在人类中，血管活性肠肽（VIP）可能在身体受热期间的反射性皮肤血管舒张中发挥作用。我们检验了这样一个假设：在囊性纤维化（CF）患者的皮肤中，一氧化氮（NO）依赖性对主动血管舒张的贡献增强，以补偿VIP水平的稀少。在2个平行方案中，将微透析纤维置于11名CF患者和12名对照者的皮肤中。在一个微透析位点灌注乳酸林格液，在第二个微透析位点灌注NG-硝基-L-精氨酸甲酯（2.7 mg/ml）。用激光多普勒血流仪监测每个位点的皮肤血流量。在方案1中，局部皮肤温度每5秒升高0.5℃至42℃，然后维持在42℃约45分钟。在方案2中，受试者穿着内衬管子的套装，灌注50℃的水，足以使口腔温度（Tor）升高0.8℃。计算皮肤血管传导率（CVC）（血流量/平均动脉压），并按最大CVC百分比（硝普钠；8.3 mg/ml）进行标度。两组对局部加热的血管舒张情况相似。CF患者和对照者在皮肤血流对局部加热反应的峰值（9±3对12±5%CVCmax；P=0.6）和平原期（45±3对35±5%CVCmax；P=0.1）阶段，CVC随NO合酶抑制的变化（Δ%CVCmax）分别相似。反射性皮肤血管舒张使CF患者（58±4%CVCmax）和对照者（53±4%CVCmax；P=0.37）的CVC增加，NO合酶抑制使CF患者（37±6%CVCmax）和对照者（35±5%CVCmax；P=0.8）的CVC降低至相似程度。因此，CF患者皮肤主动血管舒张的保留与NO依赖性血管舒张增强无关。
