Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress.
Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress.
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DOI：
10.1152/japplphysiol.00036.2002
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发表时间：
2002-12
影响因子：
3.3
通讯作者：
M. Shibasaki;T. Wilson;J. Cui;C. Crandall
中科院分区：
文献类型：
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作者：
M. Shibasaki;T. Wilson;J. Cui;C. Crandall
一氧化氮（NO）有助于活跃皮肤血管舒张在人类热应激。考虑到乙酰胆碱在全身受热时从胆碱能神经释放，再加上有证据表明乙酰胆碱通过NO机制引起血管舒张，因此在热应激时，在真皮空间释放乙酰胆碱可能有助于皮肤血管舒张。为了验证这一假设，7名受试者的皮肤血流量（SkBF）和出汗率同时通过放置在前臂背皮肤真皮间隙的三个微透析膜进行监测。第一层膜灌注乙酰胆碱酯酶抑制剂新斯的明（10微米），第二层膜灌注溶于上述新斯的明溶液（l-NAME(Neo)）中的NO合酶抑制剂N(G)-硝基-l-精氨酸甲酯（l-NAME； 10毫米），第三层膜灌注林格氏液作为对照。每位受试者通过水灌注服暴露在大约20分钟的全身加热下，平均体温从36.4 +/- 0.1℃升高到37.5 +/- 0.1℃（P < 0.05）。热应激后，每个位点的SkBF归一化到最大值，通过施用28 mM硝普钠来鉴定。与其他部位相比，新斯的明治疗部位皮肤血管舒张的平均体温阈值显著降低（新斯的明：36.6 +/- 0.1℃，l-NAME(Neo): 37.1 +/- 0.1℃，对照组：36.9 +/- 0.1℃），而l-NAME（Neo）治疗部位和对照组之间没有明显的阈值差异。热应激结束时，新斯的明处理位点与对照位点的SkBF无显著差异，而l-NAME（Neo）处理位点的SkBF显著低于其他位点。这些结果表明，胆碱能神经释放的乙酰胆碱能够在热应激早期通过NO合酶机制调节皮肤血管舒张，而不是在皮肤血管舒张之后。
Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetylcholinesterase inhibitor neostigmine (10 microM), the second membrane was perfused with the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (l-NAME(Neo)), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to approximately 20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 +/- 0.1 to 37.5 +/- 0.1 degrees C (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 +/- 0.1 degrees C, l-NAME(Neo): 37.1 +/- 0.1 degrees C, control: 36.9 +/- 0.1 degrees C), whereas no significant threshold difference was observed between the l-NAME(Neo)-treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the l-NAME(Neo)-treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation.