Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal hot flash episodes.

Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal hot flash episodes.
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DOI:
10.1097/gme.0b013e3181d674d6
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发表时间:
2010-09
期刊:
Menopause (New York, N.Y.)
影响因子:
--
通讯作者:
Crandall CG
Crandall CG
中科院分区:
其他
文献类型:
--
作者:
Hubing KA;Wingo JE;Brothers RM;Del Coso J;Low DA;Crandall CG

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本研究的目的是检验以下假设:局部抑制一氧化氮和前列腺素合成会减弱绝经后潮热期间的皮肤血管舒张反应。将四张微透析膜插入 8 名绝经后妇女的前臂皮肤(背部表面)(平均值±标准差,51±7 岁)。林格溶液(对照)、抑制前列腺素合成的 10mM 酮咯酸(Keto)、抑制一氧化氮合酶的 10mM NG-L-精氨酸甲酯(L-NAME)以及 10mM 酮 + 10mM L-NAME 的组合分别注入不同部位。使用激光多普勒血流计对每个部位的皮肤血流进行索引。皮肤血管电导 (CVC) 计算为激光多普勒通量/平均动脉血压,并表示为研究结束时在所有部位输注 50mM 硝普钠后获得的最大计算 CVC (CVCmax) 的百分比。分析了 13 次潮热的数据。在对照部位,CVC 的平均值±SD 峰值增加为 15.5±6% CVCmax 单位。该值相对于 Keto 部位 CVC 的峰值增加没有差异(13.0±5 % CVCmax 单位,P = 0.09)。然而,相对于对照和酮位点,闪光期间 CVC 的峰值增加在 L-NAME 和 L-NAME + Keto 位点(分别为 7.4±4% CVCmax 单位和 8.7±7% CVCmax 单位)减弱(两个比较的 P<0.05)。任何部位之间的出汗率峰值增加没有显着差异(P = 0.24)。这些数据表明,潮热期间的皮肤血管舒张含有一氧化氮成分。尽管前列腺素合成受到抑制,但 CVC 仍增加,这表明前列腺素在潮热期间不会导致皮肤血管舒张。
The purpose of this study was to test the hypothesis that local inhibition of nitric oxide and prostaglandin synthesis attenuates cutaneous vasodilator responses during post-menopausal hot flashes. Four microdialysis membranes were inserted into forearm skin (dorsal surface) of 8 post-menopausal women (mean ± SD, 51±7 y). Ringers solution (control), 10mM Ketorolac (Keto) to inhibit prostaglandin synthesis, 10mM NG-L-arginine methyl ester (L-NAME) to inhibit nitric oxide synthase, and a combination of 10mM Keto + 10mM L-NAME were each infused at the separate sites. Skin blood flow at each site was indexed using laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as laser-Doppler flux/mean arterial blood pressure and was expressed as a percentage of the maximal calculated CVC (CVCmax) obtained following infusion of 50mM sodium nitropruside at all sites at the end of the study. Data from 13 hot flashes were analyzed. At the control site, the mean ± SD peak increase in CVC was 15.5±6% CVCmax units. This value was not different relative to the peak increase in CVC at the Keto site (13.0±5 % CVCmax units, P = 0.09). However, the peak increase in CVC during the flash was attenuated at the L-NAME and L-NAME + Keto sites (7.4±4 % CVCmax units and 8.7±7 % CVCmax units, respectively) relative to both the control and the Keto sites (P<0.05 for both comparisons). There were no significant differences in the peak increases in sweat rate between any of the sites (P = 0.24). These data demonstrate that cutaneous vasodilation during a hot flash has a nitric oxide component. Increases in CVC despite the inhibition of prostaglandin synthesis suggest prostaglandins do not contribute to cutaneous vasodilation during a hot flash.
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