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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。
In this study, nitric oxide (NO) synthase inhibitor Nw-nitro-L-arginine methyl ester (L-NAME), NO precursor L-arginine and NO direct donor sodium nitroprusside endothelial source Regulatory Effect of Sex Relaxor (EDRF) on Vascular Tension of Pulmonary Basilar in Isolated Perfused Guinea Pigs and Its Relationship with Pulmonary Artery Pressure Induced by Platelet Activating Factor (PAF). The results showed that: L-NAME significantly increased pulmonary arterial pressure, pulmonary microvascular pressure and pulmonary artery resistance, arginine had no significant effect on basal vascular tone, but could block the changes caused by L-NAME. PAF can significantly increase pulmonary arterial pressure, pulmonary capillary pressure and pulmonary artery resistance, combined with L-NAME have a superposition effect, not blocked by L-arginine and sodium nitroprusside, indicating that the basic state of the pulmonary vascular endothelium release a certain amount of EDRF maintained Pulmonary circulation of low pressure, low resistance state. The mechanism by which PAF increases pulmonary vascular pressure and resistance is not by inhibiting the synthesis of EDRF, and EDRF does not block PAF-induced pulmonary vascular tone.