Effects of nitric oxide synthase inhibition on cutaneous vasodilation during body heating in humans.

Effects of nitric oxide synthase inhibition on cutaneous vasodilation during body heating in humans.
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一氧化氮合酶抑制对人体发热期间皮肤血管舒张的影响。

DOI:
10.1152/jappl.1998.85.3.830
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发表时间:
1998
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Joyner,MJ
Joyner,MJ
中科院分区:
--
文献类型:
--
作者:
Shastry,S;Dietz,NM;Halliwill,JR;Reed,AS;Joyner,MJ

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我们试图进一步研究一氧化氮(NO)在人体加热过程中神经介导的皮肤血管舒张中的潜在作用。六名受试者被加热的水灌注服,而皮肤血流量测量使用激光多普勒流量计放置在两个前臂。在建立了明显的皮肤血管舒张后,通过肱动脉导管选择性地向一侧前臂给予NO合酶催化剂NG-单甲基-L-精氨酸(l-NMMA)。在身体加热期间,口腔温度升高1.1 ± 0.1°C,而心率增加30 ± 6次/min。平均动脉压保持恒定在84 ± 2 mmHg。在实验前臂中,在I-NMMA输注后,皮肤血管传导性(CVC;激光多普勒)降低至对加热的峰值响应的86 ± 5%(P< 0.05相对于预I-NMMA值)。在一些受试者中,l-NMMA导致CVC下降约30%;在其他受试者中,它对皮肤循环的影响很小。对照组的CVC随着加热显示出类似的增加,然后保持恒定,而对侧给予NMMA。这些结果表明,NO有助于适度,但不一致,皮肤血管舒张人体加热过程中。它们还表明NO不是引起扩张的唯一因素。
We sought to examine further the potential role of nitric oxide (NO) in the neurally mediated cutaneous vasodilation in nonacral skin during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured by using laser-Doppler flowmeters placed on both forearms. The NO synthase inhibitorNG-monomethyl-l-arginine (l-NMMA) was given selectively to one forearm via a brachial artery catheter after marked cutaneous vasodilation had been established. During body heating, oral temperature increased by 1.1 ± 0.1°C while heart rate increased by 30 ± 6 beats/min. Mean arterial pressure stayed constant at 84 ± 2 mmHg. In the experimental forearm, cutaneous vascular conductance (CVC; laser-Doppler) decreased to 86 ± 5% of the peak response to heating (P< 0.05 vs. pre-l-NMMA values) afterl-NMMA infusion. In some subjects,l-NMMA caused CVC to fall by ∼30%; in others, it had little impact on the cutaneous circulation. CVC in the control arm showed a similar increase with heating, then stayed constant whilel-NMMA was given to the contralateral side. These results demonstrate that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans. They also indicate that NO is not the only factor responsible for the dilation.