A role for nitric oxide in active thermoregulatory vasodilation.
A role for nitric oxide in active thermoregulatory vasodilation.
复制标题
一氧化氮在主动体温调节血管舒张中的作用。
DOI：
10.1152/ajpheart.1993.264.5.h1355
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Bishop,VS
中科院分区：
文献类型：
--
作者：
Taylor,WF;Bishop,VS
我们之前已经证明，在全身加热（WBH）过程中，有意识的、长期使用仪器的兔子耳血流速度（EBF）的增加涉及活跃的神经源性血管舒张，这种舒张被局部神经阻滞所消除。本研究旨在测试一氧化氮（NO）在兔耳热疗过程中神经源性血管舒张中的潜在作用。用仪器测量家兔动脉压、心率和EBF（多普勒超声）。导管也放置在左舌动脉给药到左耳。whbh是通过放置在兔子周围的橡胶垫循环温水来实现的。用直肠热电偶测量内部温度。在whbh期间，通过舌动脉给药N - omega-硝基- l -精氨酸（L-NNA），一种生成NO的假底物（10(-5)M，共4-5 ml），以确定NO是否参与EBF的增加。在妊娠期，左耳血管导度（EVC）从0.07 +/- 0.03增加到5.87 +/- 0.73 kHz/100 mmHg，右耳EVC从0.20 +/- 0.13增加到4.49 +/- 1.73 kHz/100 mmHg。EVC最大时，左舌动脉给予L-NNA。潜伏期23 min后EVC开始下降。56 +/- 8 min时，左、右EVC分别降至0.18 +/- 0.10和0.23 +/- 0.11 kHz/100 mmHg （P < 0.05）。随后输注l -精氨酸，一氧化氮形成的真正底物，恢复EVC。这些结果表明，一氧化氮参与了兔耳加热过程中的主动血管舒张。
We have shown previously that an increase in ear blood flow velocity (EBF) in the conscious, chronically instrumented rabbit during whole body heating (WBH) involves active neurogenic vasodilation that is abolished by local nerve block. This study was designed to test the potential role of nitric oxide (NO) in rabbit ear neurogenic vasodilation during hyperthermia. Rabbits were instrumented for the measurement of arterial pressure, heart rate, and EBF (Doppler ultrasound). A catheter was also placed in the left lingual artery for administration of drugs to the left ear. WBH was achieved by circulating warm water through a rubber pad placed around the rabbit. Internal temperature was measured with a rectal thermocouple. During WBH, bolus injections of N omega-nitro-L-arginine (L-NNA), a false substrate for the formation of NO, were given via the lingual artery (10(-5) M, 4-5 ml total) to determine whether NO was involved in the increase in EBF. During WBH, left ear vascular conductance (EVC) increased from 0.07 +/- 0.03 to 5.87 +/- 0.73 kHz/100 mmHg and right EVC from 0.20 +/- 0.13 to 4.49 +/- 1.73 kHz/100 mmHg. When EVC was maximum, L-NNA was administered into the left lingual artery. EVC began to decrease after a latency of 23 min. At 56 +/- 8 min, left and right EVC had decreased to 0.18 +/- 0.10 and 0.23 +/- 0.11 kHz/100 mmHg, respectively (P < 0.05). Subsequent infusions of L-arginine, the true substrate for NO formation, restored EVC. These results suggest that NO is involved in active vasodilation during heating in the rabbit ear.