左旋精氨酸对吸入一氧化氮降低肺动脉高压的延长作用

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

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。

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 seletive decrease of pulmonary hypertention. 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(12～15ppm) for 10 minutes or inhaled NO plus venous administraed L arginine(10g), 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.