Study on the role of nitric oxide on sweating

人体皮肤血流的反射控制是通过交感缩血管神经和交感主动扩血管系统完成的。皮肤主动性血管舒张与汗腺的激活密切相关，并被认为是由胆碱能交感神经的肽能共递质（如VIP或CGRP）介导的。然而，由于缺乏动物模型，对主动血管舒张系统的作用机制尚不完全清楚。因此，我们尝试开发猫爪模型。在4只麻醉猫中，用通气胶囊法测量爪垫上的出汗，用激光多普勒流量计测量皮肤血流量。麻醉后自发汗消失。乙酰胆碱（ACh）和毛果芸香碱的局部和全身给药引起出汗，而皮肤血管舒张。电刺激胫神经引起出汗，并使后爪皮肤血管舒张。视频显微镜（× 25-175）使我们能够观察到 ...更多信息 观察到汗液从腺体孔中渗出，显示汗腺密度约为每平方毫米13-15个。这些结果表明猫爪是研究皮肤主动血管舒张机制的一种有用的动物模型。在受试者前臂腹侧给予尼古丁（10 μ <-4>g/ml，ip），测量其上臂橡皮筋外部位的出汗率和皮肤血流量，尼古丁引起轴突反射性出汗和皮肤血管扩张，两者在整个观察期内呈平行变化。先前给药的阿托品阻断尼古丁引起的出汗反应，但未能阻断同一区域的皮肤血管舒张。结果表明，皮肤血管舒张伴随轴突反射出汗可能是介导的，而不是由乙酰胆碱的毒蕈碱作用，但由一些血管舒张多肽，如VIP或CGRP共同释放的乙酰胆碱从节后泌汗神经末梢。通过在猫爪出汗模型中使用这些血管活性肽的选择性阻断剂的药物方法，期望进一步理解。少

Reflex control of skin blood flow in human is accomplished through sympathetic vasoconstrictor nerves and a sympathetic active vasodilator system. Cutaneous active vasodilation is closely related to the activation of sweat glands and is suggested to be mediated by peptidergic cotransmitters, such as VIP or CGRP, of the cholinergic sympathetic nerve. However, the mechanisms of active vasodilator system is not fully understood, because of the lack of the animal model. Therefore, we tried to develop a cat paw model. In 4 anesthetized cats, sweating on the paw pad was measured by a ventilated capsule method and skin blood flow was measured with a laser-Doppler flowmeter. Spontaneous sweating was disappeared after anesthesia. Local and systemic administration of accetylcholine (ACh) and pilocarpine induced sweating without cutaneous vasodilation. Electric stimulation of the tibial nerve induced sweating with cutaneous vasodilation on the hind paw. Video-microscope (× 25-175) enabled us to o … More bserve sweat emergence from the gland pores, and showed the sweat gland density of about 13-15 per mm^2. These results indicate that cat paw is a useful animal model to study the mechanisms of cutaneous active vasodilation. In the human subjects, on the ventral surface of the forearm nicotine (10^<-4> g/ml, ip) was administered, and sweat rate and cutaneous blood flow were measured at the sites beyond a rubber band bound around the arm. Nicotine induced axone-reflex sweating as well as skin vasodilatation, and the both responses parallely changed throughout observation period. The previously administered atropine blocked the sweating response induced by nicotine, but failed to block the cutaneous vasodilatation on the same area. The results indicate that skin vasodilatation accompanied with axone-reflex sweating is probably mediated, not by muscarinic action of a ACh, but by some vasodilative polypeptides, such as VIP or CGRP co-released with ACh from the postganglionic sudomotor nerve terminals. Further understanding is expected through the pharmaceutical approaches using selective blockers of these vasoactive peptide in the useful cat paw sweating model. Less