一氧化氮合成的抑制增强了离体大鼠肺脏中的缺氧性血管收缩。

Inhibition of nitric oxide synthesis potentiates hypoxic vasoconstriction in isolated rat lungs.

作者信息

Robertson B E, Warren J B, Nye P C

机构信息

University Laboratory of Physiology, Oxford.

出版信息

Exp Physiol. 1990 Mar;75(2):255-7. doi: 10.1113/expphysiol.1990.sp003399.

DOI:10.1113/expphysiol.1990.sp003399

PMID:2340164

Abstract

We have investigated the influence of endogenous nitric oxide (NO) on the vascular resistance of isolated rat lungs by inhibiting its synthesis with the false substrate N-monomethyl-L-arginine (L-NMMA). When perfused with blood at constant flow the addition of L-NMMA (10(-3) M) did not affect pulmonary arterial pressure in hyperoxia but did increase the response to hypoxia (PO2 25-35 mmHg) by 2.5 +/- 0.2 fold (mean +/- S.E.M.). The effect of L-NMMA was reversed by 3 x 10(-3) M-L-arginine, the true substrate for NO synthesis. Thus NO is an important pulmonary vasodilator but hypoxic vasoconstriction does not result from a reduction of its background release.

摘要

我们通过使用假底物N-单甲基-L-精氨酸（L-NMMA）抑制内源性一氧化氮（NO）的合成，研究了其对离体大鼠肺血管阻力的影响。在以恒定流量灌注血液时，添加L-NMMA（10⁻³ M）在高氧条件下不影响肺动脉压，但在低氧（PO₂ 25 - 35 mmHg）时确实使反应增加了2.5 ± 0.2倍（平均值 ± 标准误）。L-NMMA的作用可被3×10⁻³ M的L-精氨酸逆转，L-精氨酸是NO合成的真实底物。因此，NO是一种重要的肺血管扩张剂，但低氧性肺血管收缩并非源于其基础释放的减少。