Cremona G, Higenbottam T, Takao M, Hall L, Bower E A
Department of Respiratory Physiology, Papworth Hospital, Cambridge, United Kingdom.
J Appl Physiol (1985). 1995 Jan;78(1):59-63. doi: 10.1152/jappl.1995.78.1.59.
Endothelium-derived nitric oxide (NO) is an important regulator of vascular resistance. Low concentrations of NO have been recorded in the exhaled breath of spontaneously breathing animals and humans. To determine whether NO synthesis in the lung contributes to the NO measured in the breath, we measured the concentration of NO in the exhaled air of isolated perfused and ventilated porcine lungs by using a chemiluminescence method. With NO-free normoxic ventilation (21% O2-5% CO2-74% N2) of eight porcine lungs perfused with a Krebs-dextran and albumin perfusate, baseline exhaled NO was 5.8 +/- 1.8 parts per billion (ppb) and pulmonary vascular resistance (PVR) was 8.9 +/- 1.8 mmHg.l-1.min. Hypoxic ventilation (5% O2-5% CO2-90% N2) caused a fall in NO to 3.6 +/- 1.8 ppb and a rise in PVR to 13.6 +/- 3.6 mmHg.l-1.min. Vasoconstriction with the thromboxane analogue U-46619 (10(-9) M) raised PVR to 31.7 +/- 6.8 mmHg.l-1.min but did not decrease NO levels from baseline. Subsequent addition of acetylcholine (10(-6)M) lowered PVR to 22.1 +/- 4.5 mmHg.l-1.min and increased exhaled NO to 7.0 +/- 2.0 ppb. Addition of a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (10(-5) M), to four lungs caused a rise in PVR to 43.0 +/- 7.0 mmHg.l-1.min and a decrease in NO to 1.5 +/- 1.0 ppb. Addition of autologous blood to the perfusate of four lungs caused no change in PVR from baseline but decreased exhaled NO to 2.7 +/- 0.5 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)
内皮衍生的一氧化氮（NO）是血管阻力的重要调节因子。在自主呼吸的动物和人类呼出的气体中已检测到低浓度的NO。为了确定肺中NO的合成是否对呼出气体中测得的NO有贡献，我们使用化学发光法测量了离体灌注和通气的猪肺呼出气体中NO的浓度。用不含NO的常氧通气（21%O₂-5%CO₂-74%N₂）对8个用Krebs-葡聚糖和白蛋白灌注液灌注的猪肺进行通气，呼出气体中NO的基线水平为5.8±1.8十亿分之一（ppb），肺血管阻力（PVR）为8.9±1.8 mmHg·l⁻¹·min。低氧通气（5%O₂-5%CO₂-90%N₂）使NO降至3.6±1.8 ppb，PVR升至13.6±3.6 mmHg·l⁻¹·min。用血栓素类似物U-46619（10⁻⁹ M）进行血管收缩使PVR升至31.7±6.8 mmHg·l⁻¹·min，但未使NO水平低于基线。随后加入乙酰胆碱（10⁻⁶M）使PVR降至22.1±4.5 mmHg·l⁻¹·min，并使呼出气体中NO增加至7.0±2.0 ppb。向4个肺中加入一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（10⁻⁵ M）使PVR升至43.0±7.0 mmHg·l⁻¹·min，NO降至1.5±1.0 ppb。向4个肺的灌注液中加入自体血，PVR与基线相比无变化，但呼出气体中NO降至2.7±0.5 ppb。（摘要截短于250字）
