PERMISSIVE ROLE FOR NITRIC-OXIDE IN ACTIVE THERMOREGULATORY VASODILATION IN RABBIT EAR
PERMISSIVE ROLE FOR NITRIC-OXIDE IN ACTIVE THERMOREGULATORY VASODILATION IN RABBIT EAR
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DOI：
10.1152/ajpheart.1995.269.5.h1613
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发表时间：
1995-11-01
影响因子：
4.8
通讯作者：
BISHOP, VS
中科院分区：
文献类型：
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作者：
FARRELL, DM;BISHOP, VS
本研究的目的是测试的假设，即在全身加热（WBH），一氧化氮（NO）在内皮细胞中合成的协同作用与未知的神经递质引起主动血管舒张。测量家兔的平均动脉压、心率和耳血流量（EBF）（多普勒超声）。在WBH期间，通过舌动脉导管给予NO-硝基-L-精氨酸甲酯（L-NAME，10-40 mg，10-15 min，n = 6只兔;组1），一种NO合酶抑制剂，或皂苷（30-40 mg，10-20 min，n = 6只兔;组2），一种剥脱内皮的去污剂，直到体温调节血管舒张逆转。当EBF稳定在新的降低水平时，经舌动脉导管输注NO供体硝普钠（SNP）（0.2- 1.0mg/ml，0.01- 0.05ml/min，2-5 min）。在WBH期间，第2组的EBF从0.39 +/- 0.08增加到6.47 +/- 0.63 kHz，从0.69 +/- 0.18增加到5.72 +/- 0.49 kHz。第二组。输注L-NAME使第1组的EBF降低至1.97 +/- 0.40 kHz。输注皂苷使第2组的EBF降低至1.23 +/- 0.40 kHz。随后在高热期间输注SNP使第2组的EBF恢复至6.88 +/- 0.72 kHz，第2组为5.53 +/- 1.27 kHz，但在常温下给药时没有效果。这些结果表明，NO的行为与另一种物质，大概是WBH上释放的神经递质，引起温度调节血管舒张。
The present study was designed to test the hypothesis that during whole body heating (WBH), nitric oxide (NO) synthesized in the endothelium acts synergistically with an unknown neurotransmitter to elicit active vasodilation. Rabbits were instrumented for the measurement of mean arterial pressure, heart rate, and ear blood flow (EBF) (Doppler ultrasound). During WBH, either No-nitro-L-arginine methyl ester (L-NAME, 10-40 mg over 10-15 min, n = 6 rabbits; group 1), a NO synthase inhibitor, or saponin (30-40 mg over 10-20 min, n = 6 rabbits; group 2), a detergent that denudes the endothelium, was given via a lingual artery catheter until thermoregulatory vasodilation was reversed. When EBF stabilized at the new reduced level, the NO donor, sodium nitroprusside (SNP), was infused (0.2-1.0 mg/ml, 0.01-0.05 ml/min, 2-5 min) via the lingual artery catheter. During WBH, EBF increased from 0.39 +/- 0.08 to 6.47 +/- 0.63 kHz in group 2, and from 0.69 +/- 0.18 to 5.72 +/- 0.49 kHz. in group 2. Infusion of L-NAME decreased EBF in group 1 to 1.97 +/- 0.40 kHz. Infusion of saponin decreased EBF in group 2 to 1.23 +/- 0.40 kHz. Subsequent SNP infusion during hyperthermia returned EBF to 6.88 +/- 0.72 kHz in group 2 and 5.53 +/- 1.27 kHz ingroup 2 but had no effect when administered during normothermia. These results suggest that NO acts in conjunction with another substance, presumably the neurotransmitter released on WBH, to elicit thermoregulatory vasodilation.