左旋精氨酸对吸入一氧化氮降低肺动脉高压的延长作用

目的观察一氧化氮底物左旋精氨酸（Ｌａｒｇ）延长吸入一氧化氮（ＮＯ）选择性降低肺动脉高压过程中的作用。方法８只猪麻醉后制成急性缺氧性肺动脉高压模型，在ＳｗａｎＧａｎｚ导管和动脉导管监测下吸入ＮＯ（１２～１５ｐｐｍ）的过程中静脉注入Ｌａｒｇ（共１０ｇ），观察停用ＮＯ后体循环和肺循环血流动力学的变化情况。结果单纯吸入ＮＯ能选择性降低急性缺氧性肺动脉高压，肺动脉压力从４２±０４ｋＰａ降至２５±０５ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ，Ｐ＜０．０１），肺血管阻力从５６±２５ｋＰａ·ｓ·Ｌ１降至３１±１３ｋＰａ·ｓ·Ｌ－１（Ｐ＜０．０１），但持续时间短；ＮＯ吸入加静脉注射Ｌａｒｇ没有使肺动脉压进一步下降，但能显著延长吸入ＮＯ对肺动脉压的降压时间（２０倍），对体循环血压则无影响。结论提供内源性ＮＯ的底物Ｌａｒｇ能延长ＮＯ的降压作用，提示急性缺氧时ＮＯ的生成可能有相对不足。

L arginine prolonged the efficacy of inhaled nitric oxide on the inhibition of pulmonary hypertension

OBJECTIVE: The aim of this study is to investigate the effects of L-arginine, the substrate of nitric oxide (NO) on the duration of nitric oxide selective decrease of pulmonary hypertension. To assess whether combined use of inhaled nitric oxide and venous administered L-arginine can improve the efficacy of inhaled NO on the inhibition of hypoxia induced pulmonary hypertension. METHOD: Eight pigs with hypoxic pulmonary hypertension received either inhaled NO(12-15 ppm) for 10 minutes or inhaled NO plus venous administrered L-arginine(10 g), then hemodynamic parameters were recorded. RESULT: NO inhalation significantly inhibited hypoxic induced pulmonary hypertension with pulmonary arterial pressure decreasing from 4.2 +/- 0.4 kPa to 2.5 +/- 0.5 kPa(P < 0.01) and pulmonary vascular resistance from 56 +/- 25 kPa.s.L-1 to 31 +/- 13 kPa.s.L-1(P < 0.01), but this just lasted for 3-5 minutes after stopping inhalation; combined use of L-arginine infusion did not further decrease pulmonary arterial pressure, but significantly prolonged the inhibitory effect of inhaled NO on pulmonary hypertension (20 times) as compared with inhaled NO only. CONCLUSION: With the existence of exogenous NO, supplement of NO substrate L-arginine produced a synesgetic inhibition effect on hypoxic induced pulmonary hypertension.