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Study on the role of nitric oxide on sweating

一氧化氮对出汗作用的研究

基本信息

批准号：
11670077
负责人：
MATSUMOTO Takaaki
金额：
$ 2.3万
依托单位：
Aichi Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

项目摘要

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

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主动血管舒张系统完成的。皮肤主动血管舒张与汗腺的激活密切相关，并且被认为是由胆碱能交感神经的肽能共递质（例如 VIP 或 CGRP）介导的。然而，由于缺乏动物模型，主动血管舒张系统的机制尚不完全清楚。因此，我们尝试开发猫爪模型。在 4 只麻醉猫中，通过通气胶囊法测量爪垫上的出汗情况，并使用激光多普勒流量计测量皮肤血流量。麻醉后自汗消失。局部和全身给予乙酰胆碱（ACh）和毛果芸香碱诱导出汗，但不引起皮肤血管舒张。胫神经的电刺激引起出汗，后爪上的皮肤血管舒张。视频显微镜（×25-175）使我们能够观察汗腺从腺孔中的排出，并显示汗腺密度约为每mm^2 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有用动物模型。在人类受试者中，在前臂的腹侧表面施用尼古丁(10 1 -4 g/ml，ip)，并在围绕手臂的橡皮筋之外的部位测量出汗率和皮肤血流量。尼古丁诱导轴突反射性出汗以及皮肤血管舒张，并且这两种反应在整个观察期间平行变化。先前施用的阿托品可以阻断尼古丁引起的出汗反应，但无法阻断同一区域的皮肤血管舒张。结果表明，伴随轴突反射性出汗的皮肤血管舒张可能不是由ACh的毒蕈碱作用介导的，而是由一些血管舒张多肽介导的，例如与ACh从节后催汗神经末梢共同释放的VIP或CGRP。预计通过在有用的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可以进一步了解。较少的