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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?