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血管收缩神经和交感活性血管扩张系统完成的。皮肤主动血管扩张与汗腺的激活密切相关，被认为是由胆碱能交感神经肽能共递质，如VIP或CGRP所介导的。然而，由于缺乏动物模型，目前对活性血管扩张系统的作用机制尚不完全清楚。因此，我们试图开发一种猫爪模型。在4只麻醉猫上，用呼吸胶囊法测量爪垫出汗，用激光多普勒血流计测量皮肤血流量。麻醉后自汗消失。局部和全身应用乙酰胆碱(ACh)和匹罗卡品可引起无皮肤血管扩张的出汗。电刺激胫神经引起出汗，后爪皮肤血管扩张。视频显微镜(×25-175)使我们能够看到…腺孔出汗较多，汗腺密度约为13-15个/mm~2。这些结果表明，猫爪是研究皮肤主动血管扩张机制的有用动物模型。在受试者的前臂腹侧表面注射尼古丁(10~(-4)g/ml，ip)，并在手臂上绑有橡皮筋的部位测量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，这两种反应在整个观察期内平行变化。之前给药的阿托品阻断了尼古丁引起的出汗反应，但未能阻止同一区域的皮肤血管扩张。结果表明，皮肤血管扩张伴随轴索反射性出汗可能不是由ACh的毒鼠碱作用所介导的，而是由节后舒缩运动神经末梢释放的VIP或CGRP等扩血管多肽介导的。通过在有用的猫爪出汗模型中使用这些血管活性多肽的选择性阻滞剂的药物方法，有望进一步了解。较少

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