内皮源性舒张因子对肺血管张力的调节及其与血小板激活因子引起肺动脉压升高的关系

本实验采用一氧化氮（ＮＯ）合成酶抑制剂Ｎｗ－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ）、ＮＯ前体Ｌ－精氨酸和ＮＯ直接供体硝普钠研究内皮源性舒张因子（ＥＤＲＦ）对离体灌注豚鼠肺基础血管张力的调节作用及其与血小板激活因子（Ｐｌａｔｅｌｅｔ－ａｃｔｉｖａｔｉｎｇｆａｃｔｏｒ，ＰＡＦ）所致肺动脉压增高的关系。结果表明：Ｌ－ＮＡＭＥ可以明显增高肺动脉压、肺微血管压和肺动脉阻力，精氨酸对基础血管张力没有明显影响，但可阻断Ｌ－ＮＡＭＥ引起的变化。ＰＡＦ可明显增高肺动脉压、肺微血管压和肺动脉阻力，与Ｌ－ＮＡＭＥ合用有叠加效应，不被Ｌ－精氨酸和硝普钠阻断，说明基础状态下肺血管内皮释放一定量的ＥＤＲＦ维持肺循环的低压、低阻状态。ＰＡＦ增高肺血管压力和阻力的机制不是通过抑制ＥＤＲＦ合成的途径，ＥＤＲＦ不能阻断ＰＡＦ引起的肺血管张力升高。

Modulation of Pulmonary Vascular Tone by Endothelium-derived Relaxing Factor and Its Correlation with Platelet-activating Factor Induced Pulmonary Hypertension

Using NO synthase inhibitor Nw-nitro-L-arginine methyl ester(L-NAME),NO progenitor L-arginine and NO donor sodium nitroprusside(SNP),we investigated EDRF modulation of baseline vessel tone in isolated perfused guinea-pig lungs. The relationship between EDRF and pulmonary hypertension induced by platelet-activating factor(PAF)was also studied.The results revealed that L-NAME obviously increased pulmonary arterial pressure,microvascular pressure and arterial resistance.L-Arginine had no prominent influence on basal vessel tone itself but blocked L-NAME induced changes.PAF increased pulmonary arterial pressure,microvascular pressure and arterial resistance significantly.The effects were added by the combination of L-NAME,and unblocked by L-arginine and SNP,indicating that under basal state,EDRF was released from pulmonary vascular endothelium to maintain low pressure,low resistance in pulmonary circulation.The mechanism by which PAF increased pulmonary vascular pressure and resistance was not through inhibition of EDRF synthesis.EDRF did not block PAF-induced changes in pulmonary vascular tone.