Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.
Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.
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内源性一氧化氮可能是肺循环和体内缺氧升压反应的调节剂。
DOI：
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
P. Hedqvist
中科院分区：
文献类型：
--
作者：
M. Persson;L. Gustafsson;N. Wiklund;S. Moncada;P. Hedqvist
本研究的目的是探讨由L-精氨酸形成的内源性一氧化氮在体内肺循环调节中的作用，特别是在缺氧性升压反应中的作用。在人工呼吸的开胸兔中，常氧(FiO2=21%)时的肺血管阻力为78+/-16cmH2O ml-1min 1000-1(MRUL)。低氧(FiO2=10%)使肺血管阻力增加至117+/-17mRUL。一氧化氮合酶抑制剂N omega-硝基-L-精氨酸甲酯(L-NAME)使肺血管阻力在常氧时增加到192+/-28mRUL，在低氧时增加到462+/-80mRUL。在N-硝基-L-精氨酸甲酯输注过程中，平均动脉压升高，心输出量下降，在低氧机械通气时更为明显。L-精氨酸逆转N-奥米伽-硝基-L-精氨酸甲酯对肺血管阻力的影响，常氧通气组为140±26mRUL，低氧通气组为239+/-42mRUL。在自主呼吸的闭胸兔，N-硝基-L-精氨酸甲酯引起动脉血氧分压显著降低，呼吸频率和中心静脉压增加，而血pH、二氧化碳分压和碱过量无明显变化。综上所述，提示由L-精氨酸生成的内源性一氧化氮可能是常氧肺通气-灌流匹配的调节因子，而一氧化氮则是缺氧性升压反应的内源性调节剂。
The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (FIO2 = 21%) was 78 +/- 16 cmH2O ml-1 min 1000-1 (mRUL). Hypoxic ventilation (FIO2 = 10%) increased pulmonary vascular resistance to 117 +/- 17 mRUL. N omega-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 +/- 28 mRUL and during hypoxic ventilation to 462 +/- 80 mRUL. During N omega-nitro-L-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N omega-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 +/- 26 mRUL and at hypoxic ventilation to 239 +/- 42 mRUL. In spontaneously breathing closed-chest rabbits, N omega-nitro-L-arginine methylester evoked a marked decrease in arterial PO2 and increases in respiration frequency and central venous pressure, while blood pH, PCO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.
DOI：
10.1073/pnas.84.24.9265
发表时间：
1987-12-01
影响因子：
11.1
作者：
IGNARRO, LJ;BUGA, GM;CHAUDHURI, G
通讯作者：
CHAUDHURI, G
影响因子：
15.9
作者：
BRASHERS, VL;PEACH, MJ;ROSE, CE
通讯作者：
ROSE, CE
DOI：
10.1073/pnas.85.22.8664
发表时间：
1988-11-01
影响因子：
11.1
作者：
SAKUMA, I;STUEHR, DJ;LEVI, R
通讯作者：
LEVI, R