Shastry S, Minson C T, Wilson S A, Dietz N M, Joyner M J
Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
J Appl Physiol (1985). 2000 Feb;88(2):467-72. doi: 10.1152/jappl.2000.88.2.467.
We sought to investigate further the roles of sweating, ACh spillover, and nitric oxide (NO) in the neurally mediated cutaneous vasodilation during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured with a laser-Doppler flowmeter. After a rise in core temperature (1. 0 +/- 0.1 degrees C) and the establishment of cutaneous vasodilation, atropine and subsequently the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) were given to the forearm via a brachial artery catheter. After atropine infusion, cutaneous vascular conductance (CVC) remained constant in five of six subjects, whereas L-NAME administration blunted the rise in CVC in three of six subjects. A subsequent set of studies using intradermal microdialysis probes to selectively deliver drugs into forearm skin confirmed that atropine did not affect CVC. However, perfusion of L-NAME resulted in a significant decrease in CVC (37 +/- 4%, P < 0.05). The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.
我们试图进一步研究出汗、乙酰胆碱溢出以及一氧化氮（NO）在人体体温升高期间神经介导的皮肤血管舒张中的作用。六名受试者穿着水灌注服受热，同时用激光多普勒血流仪测量皮肤血流量。在核心体温升高（1.0±0.1℃）并建立皮肤血管舒张后，通过肱动脉导管向前臂给予阿托品，随后给予NO合酶抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME）。注入阿托品后，六名受试者中有五名的皮肤血管传导率（CVC）保持恒定，而给予L-NAME后，六名受试者中有三名的CVC升高受到抑制。随后使用皮内微透析探针将药物选择性地输送到前臂皮肤的一组研究证实，阿托品不影响CVC。然而，灌注L-NAME导致CVC显著降低（37±4%，P<0.05）。结果表明，出汗和通过毒蕈碱受体激活释放NO对于维持人体受热期间的皮肤扩张均非必需。
