2 med. Dept., Rudolfstiftung, Juchgasse 25, A-1030 Vienna, Austria.
Am J Physiol Lung Cell Mol Physiol. 2013 Oct 1;305(7):L485-90. doi: 10.1152/ajplung.00087.2013. Epub 2013 Jul 26.
The use of fractional exhaled nitric oxide (FeNO) has been suggested as a quantitative marker for pulmonary arterial hypertension (PAH) in humans. To further characterize FeNO in PAH we investigated this marker in a rodent model. Since there is no standardized technique for FeNO measurement in animals, we intended to reduce measuring errors and confounders of an existing published method by mathematical modification and tested its applicability in an NO-regulating therapy concept of PAH. Thirty-three male Sprague-Dawley rats underwent unilateral pneumonectomy and monocrotaline (MCT) injection and were observed for 49 days. A telemetric catheter was introduced into the left pulmonary artery to continuously record mean pulmonary arterial pressure (mPAP), and FeNO was assessed. After 35 days, animals were randomized to receive either oral l-arginine (300 mg/kg) in combination with tetrahydrobiopterin (20 mg/kg) therapy (n = 12) or vehicle (n = 11) daily over a period of 14 days. mPAP at baseline was 17.19 ± 9.62 mmHg, which increased to 53.1 ± 10.63 mmHg 28 days after monocrotaline exposure (P < 0.001). Using the modified technique, we found an inverse correlation between exhaled NO and pulmonary pressures before (r = -0.366, P = 0.043) and after MCT (r = -0.363, P = 0.038) as well as after therapy administration (r = -0.657, P = 0.02). Our modified technique proved robust in a rodent model, since valid and reproducible data were gained and showed an inverse correlation between exhaled NO and mPAP, whereas the existing method did not.
呼气一氧化氮(FeNO)的应用已被认为是人类肺动脉高压(PAH)的定量标志物。为了进一步研究 PAH 中的 FeNO,我们在啮齿动物模型中研究了这种标志物。由于目前尚无用于动物的 FeNO 测量的标准化技术,我们打算通过数学修正来减少现有发表方法的测量误差和混杂因素,并测试其在 PAH 的一氧化氮调节治疗概念中的适用性。33 只雄性 Sprague-Dawley 大鼠接受单侧肺切除术和单环素来那度胺(MCT)注射,并观察 49 天。将遥测导管引入左肺动脉,以连续记录平均肺动脉压(mPAP),并评估 FeNO。35 天后,动物随机分为接受口服 l-精氨酸(300mg/kg)联合四氢生物蝶呤(20mg/kg)治疗(n = 12)或每日载体(n = 11)治疗 14 天。基线 mPAP 为 17.19 ± 9.62mmHg,MCT 暴露 28 天后增加至 53.1 ± 10.63mmHg(P < 0.001)。使用改良技术,我们发现呼气一氧化氮与肺压在 MCT 暴露前(r = -0.366,P = 0.043)和暴露后(r = -0.363,P = 0.038)以及治疗后存在负相关给药(r = -0.657,P = 0.02)。我们的改良技术在啮齿动物模型中证明是稳健的,因为获得了有效和可重复的数据,并显示呼气一氧化氮与 mPAP 之间存在负相关,而现有方法则没有。