Nitric oxide and cutaneous active vasodilation during heat stress in humans
Nitric oxide and cutaneous active vasodilation during heat stress in humans
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DOI：
10.1152/jappl.1998.85.3.824
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发表时间：
1998-09-01
影响因子：
3.3
通讯作者：
Johnson, JM
中科院分区：
文献类型：
--
作者：
Kellogg, DL;Crandall, CG;Johnson, JM
一氧化氮(NO)是否参与人体高温时皮肤的主动血管扩张尚不清楚。我们测试了7名健康受试者在热应激(水灌洗服)过程中NO在这一过程中的作用。前臂的两个部位用皮内微透析探头进行检测。将一氧化氮合酶抑制剂N-G-硝基-L-精氨酸甲酯(N-G-硝基-L-精氨酸甲酯，简称N-G-硝基-硝基-精氨酸甲酯，简称N-硝基-硝基-精氨酸甲酯)注入林格液中，以消除NO的产生。另一处仅用林格液灌流。在这些部位同时连续监测皮肤血流量(激光多普勒血流仪)和出汗率。根据激光多普勒血流计和平均动脉压计算的皮肤血管电导，通过微透析探头与NO供体硝普钠进行灌流，使其正常化至最大水平。在常温条件下，L-NAME没有显著降低皮肤血管传导性。在热疗期间，皮肤温度保持在38-38.5摄氏度，内部温度从36.66+/-0.10摄氏度上升到37.34+/-0.06摄氏度(P<；0.01)。在热应激期间，未处理部位的皮肤血管传导性从最大值的12+/-2增加到44+/-5%，而L处理的部位仅从最大值的13+/-2增加到30+/-5%(P<；0.05)。L的名字对出汗率没有影响(P>；0.05)。因此，皮肤主动血管扩张需要功能性一氧化氮合酶来实现充分表达。
Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions, L-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38-38.5 degrees C, internal temperature rose from 36.66 +/- 0.10 to 37.34 +/- 0.06 degrees C (P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 +/- 2 to 44 +/- 5% of maximum, but only rose from 13 +/- 2 to 30 +/- 5% of maximum at L-NAME-treated sites (P < 0.05 between sites) during heat stress. L-NAME had no effect on sweat rate (P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.