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目的：检测ＮＯ与Ｏ－·２共同或分别作用对兔肺动脉反应性变化的影响。方法：将制备的离体兔肺动脉环分为ＮＯ组，Ｏ－·２组，ＮＯ＋Ｏ－·２组和溶剂对照（ＮＳ）组。用离体血管环技术观察肺动脉对乙酰胆碱（ＡＣｈ）、Ｃａ２＋载体Ａ２３１８７和苯肾上腺素（ＰＥ）的反应性变化。结果：肺动脉对ＡＣｈ的舒张反应（ｇｔｅｎｓｉｏｎ／ｍｇｄｗ）和舒张反应百分率（％），在Ｏ－·２组明显降低（Ｐ＜０．０１，与ＮＳ组比较）；在ＮＯ＋Ｏ－·２组显著高于Ｏ－·２组（Ｐ＜０．０５），但与ＮＳ组也有明显差异（Ｐ＜０．０５）；在ＮＯ组肺动脉的舒张反应接近ＮＳ组，与Ｏ－·２组有明显差异（Ｐ＜０．０５）。对Ａ２３１８７的舒张反应（用占预收缩的百分比表示），在ＮＳ、ＮＯ＋Ｏ－·２和Ｏ－·２组分别为７３．６７％，６４．８６％和５９．２６％。各组肺动脉对ＰＥ的收缩反应大致相同。Ｌ－精氨酸预孵育后，对ＰＥ的收缩反应在ＮＯ＋Ｏ－·２组收缩降低，为预孵育前收缩的５３．８９％；而在Ｏ－·２组无明显变化。结论：Ｏ－·２损害了肺动脉的内皮依赖和受体依赖性舒张反应；ＮＯ同时生成时可部分逆转Ｏ－·２的损伤作用；Ｏ－·２似通过清除内源性ＮＯ或直接累及ｅｃＮＯＳ，而发挥其损伤?
Objective: To investigate the effect of NO and O · 2 on the pulmonary reactivity in rabbits. Methods: The isolated rabbit pulmonary artery rings were divided into NO group, O 2 group, NO + O 2 group and solvent control (NS) group. The changes of reactivity of pulmonary arteries to acetylcholine (ACh), Ca2 + carrier A23187 and phenylephrine (PE) were observed by means of isolated vascular rings. RESULTS: The pulmonary arterial diastolic response (gtension / mgdw) and relaxation response (%) to ACh were significantly lower in the O-2 group (P <0.01 vs NS group) and significantly higher in the NO + O-2 group (P <0.05), but there was also significant difference with NS group (P <0.05). In the NO group, the relaxation of the pulmonary artery in the NO group was similar to that in the NS group, which was significantly different from that in the O 2 group (P < P <0.05). The relaxation response to A23187, expressed as a percentage of pre-contraction, was 73.67%, 64.86% and 59.26% for the NS, NO + O- 2 and O-2 groups, respectively. Each group of pulmonary artery contractions of PE almost the same response. After preincubation with L-arginine, the contractile response to PE decreased in NO + O- · 2 group, which was 53.89% of the contraction before pre-incubation, while there was no significant change in O-2 group. Conclusion: O 2 damages the endothelium-dependent and receptor-dependent vasodilatation of pulmonary arteries, while NO production partially reverses the damaging effect of O-2. O-2 may be mediated by clearance of endogenous NO or ecNOS , But to play its damage?