Cyclooxygenase inhibition does not alter methacholine-induced sweating
Cyclooxygenase inhibition does not alter methacholine-induced sweating
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DOI：
10.1152/japplphysiol.00644.2014
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发表时间：
2014-11-01
影响因子：
3.3
通讯作者：
Kenny, Glen P.
中科院分区：
文献类型：
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作者：
Fujii, Naoto;McGinn, Ryan;Kenny, Glen P.
胆碱能药物（如甲胆碱）可引起皮肤血管扩张和出汗。报告表明，一氧化氮（NO），环氧合酶（COX），或两者都可以促进胆碱能皮肤血管舒张。此外，据报道一氧化氮与胆碱能出汗有关；然而，COX是否与胆碱能性出汗有关尚不清楚。对10名健康青年（24 +/- 4岁）成人（7男3女）进行前臂出汗率（通气胶囊）和皮肤血管传导（CVC，激光多普勒灌注单位/平均动脉压）的评估，这些人通过皮内微透析持续灌注1)乳酸林格氏（对照），2)10 mM酮洛酸（非选择性COX抑制剂），3)10 mM n - g -硝基- l -精氨酸甲酯（L-NAME，非选择性NO合酶抑制剂）。或4)10mm酮罗拉酸+ 10mm L-NAME的组合。在四个皮肤部位，以剂量依赖的方式同时输注甲胆碱（1,10,100,1,000,2,000 mM）。与对照组相比，酮洛酸在整个治疗过程中对前臂CVC没有影响（P < 0.05），而L-NAME和酮洛酸+ L-NAME降低了10 mM甲胆碱及以上的前臂CVC （P < 0.05）。相反，治疗部位对前臂出汗无主要影响（P = 0.488），甲胆碱剂量与治疗部位对前臂出汗无交互作用（P = 0.711）。因此前臂出汗（mg.min(-1)）。从基线到最大甲胆碱剂量在4个位点之间没有差异（在2000 mM，对照0.50 +/- 0.23，酮咯酸0.44 +/- 0.23,L-NAME 0.51 +/- 0.22，酮咯酸+ L-NAME 0.51 +/- 0.23）。我们发现NO合成酶和COX抑制均不影响1-2,000 mM甲胆碱诱导的胆碱能出汗。
Cholinergic agents (e. g., methacholine) induce cutaneous vasodilation and sweating. Reports indicate that either nitric oxide (NO), cyclooxygenase (COX), or both can contribute to cholinergic cutaneous vasodilation. Also, NO is reportedly involved in cholinergic sweating; however, whether COX contributes to cholinergic sweating is unclear. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC, laser-Doppler perfusion units/mean arterial pressure) were evaluated in 10 healthy young (24 +/- 4 yr) adults (7 men, 3 women) at four skin sites that were continuously perfused via intradermal microdialysis with 1) lactated Ringer (control), 2) 10 mM ketorolac (a nonselective COX inhibitor), 3) 10 mM N-G-nitro-L-arginine methyl ester (L-NAME, a nonselective NO synthase inhibitor), or 4) a combination of 10 mM ketorolac + 10 mM L-NAME. At the four skin sites, methacholine was simultaneously infused in a dose-dependent manner (1, 10, 100, 1,000, 2,000 mM). Relative to the control site, forearm CVC was not influenced by ketorolac throughout the protocol (all P > 0.05), whereas L-NAME and ketorolac + L-NAME reduced forearm CVC at and above 10 mM methacholine (all P < 0.05). Conversely, there was no main effect of treatment site (P = 0.488) and no interaction of methacholine dose and treatment site (P = 0.711) on forearm sweating. Thus forearm sweating (in mg.min(-1).cm(-2)) from baseline up to the maximal dose of methacholine was not different between the four sites (at 2,000 mM, control 0.50 +/- 0.23, ketorolac 0.44 +/- 0.23, L-NAME 0.51 +/- 0.22, and ketorolac + L-NAME 0.51 +/- 0.23). We show that both NO synthase and COX inhibition do not influence cholinergic sweating induced by 1-2,000 mM methacholine.