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首页> 外文期刊>The journal of alternative and complementary medicine: research on paradigm, practice, and policy >Inhibition of nitric oxide synthase attenuates cutaneous vasodilation during warm moxibustion-like thermal stimulation in humans
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Inhibition of nitric oxide synthase attenuates cutaneous vasodilation during warm moxibustion-like thermal stimulation in humans

机译：一氧化氮合酶的抑制作用减弱了人体像温灸一样的热刺激过程中的皮肤血管舒张作用

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Objectives: This study investigated if nitric oxide (NO) and/or prostaglandin (PG) are responsible for cutaneous vasodilation during warm moxibustion-like thermal stimulation (WMTS). Design: For two protocols, two microdialysis membranes were placed in the medial forearm skin. In the first protocol (n=8), the sites were randomly assigned and perfused with N G-nitro-l-arginine methyl ester hydrochloride (l-NAME), an NO synthase inhibitor or Ringer's solution (control site). Similarly, two microdialysis membranes were placed in the medial forearm skin in the second protocol (n=6). One site was perfused with ketorolac (Keto), the cyclo-oxygenase (COX) pathway inhibitor, and the other site was perfused with Ringer's solution (control site). In both protocols, cutaneous vasodilation was induced using WMTS with an electronic warm moxibustion treatment appliance. After 10 minutes of baseline recording, WMTS was applied to the forearm skin for 20 minutes and recovery was monitored over a period of 20 minutes. Skin blood flow (SkBF) at each site was measured using laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as laser-Doppler flux/mean arterial blood pressure (BP). Settings/location: The study was conducted in a laboratory at the Kansai University of Health Sciences. Subjects: The subjects were 14 healthy male volunteers. Interventions: WMTS was applied to the medial forearm skin using an electronic warm moxibustion treatment appliance. Outcome measures: SkBF, skin temperature (Tsk), core body temperature (Tc), heart rate (HR), and BP were outcome measures. Results: In the first protocol, peak CVC values during WMTS at the site perfused with l-NAME were significantly decreased, compared to those at the control site (p0.05). In the second protocol, peak CVC values during WMTS did not differ between the control site and the Keto site (p0.05). Conclusions: These data demonstrate that NO is involved in the mechanism of cutaneous vasodilation induced by WMTS. Furthermore, increases in CVC despite inhibition of the COX pathway suggest that PG does not contribute to cutaneous vasodilation during WMTS.
机译：目的：本研究调查了一氧化氮（NO）和/或前列腺素（PG）在温暖的像艾灸般的热刺激（WMTS）期间是否引起皮肤血管舒张。设计：对于两种方案，在前臂内侧皮肤中放置两块微透析膜。在第一个协议中（n = 8），随机分配这些位点，并用N G-硝基-1-精氨酸甲酯盐酸盐（1-NAME），NO合酶抑制剂或林格氏液（对照位点）灌注。类似地，在第二方案中，将两个微渗析膜置于前臂内侧皮肤中（n = 6）。一个位点用酮咯酸（Keto），环加氧酶（COX）途径抑制剂灌注，另一位点用林格氏液灌注（对照位点）。在这两种方案中，均使用WMTS和电子温灸治疗仪诱导皮肤血管舒张。基线记录10分钟后，将WMTS应用于前臂皮肤20分钟，并在20分钟内监测恢复情况。使用激光多普勒血流仪测量每个部位的皮肤血流量（SkBF）。皮肤血管电导率（CVC）计算为激光多普勒通量/平均动脉血压（BP）。设置/位置：该研究在关西健康科学大学的实验室中进行。受试者：受试者为14名健康男性志愿者。干预措施：使用电子温灸治疗仪将WMTS应用于前臂内侧皮肤。结果指标：SkBF，皮肤温度（Tsk），核心体温（Tc），心率（HR）和BP是结果指标。结果：在第一个协议中，与对照位点相比，在灌注I-NAME的位点发生WMTS期间的CVC峰值显着降低（p <0.05）。在第二种方案中，WMTS期间的CVC峰值在对照位点和Keto位点之间没有差异（p> 0.05）。结论：这些数据表明NO参与WMTS诱导的皮肤血管舒张的机制。此外，尽管抑制了COX途径，但CVC的增加表明PG在WMTS期间无助于皮肤血管舒张。

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