Altered contractile sensitivity of isolated bronchial artery to phenylephrine in ovalbumin-sensitized rabbits.
Altered contractile sensitivity of isolated bronchial artery to phenylephrine in ovalbumin-sensitized rabbits.
复制标题
改变卵清蛋白致敏兔离体支气管动脉对去氧肾上腺素的收缩敏感性。
DOI：
10.1152/jappl.1999.86.5.1721
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Wanner,A
中科院分区：
文献类型：
--
作者：
Zschauer,AO;Sielczak,MW;Wanner,A
我们检验了特应性和/或过敏性肺部炎症增强α1肾上腺素受体介导的支气管动脉收缩的假设。支气管动脉阻力血管分离自经历了全身性卵清蛋白（OVA）致敏然后盐水气溶胶激发（OVA/盐水兔），或OVA致敏然后OVA气溶胶激发（OVA/OVA兔），或无致敏然后盐水气溶胶激发（对照兔）的兔。在OVA/OVA兔中，支气管肺泡灌洗和肺组织学显示淋巴细胞和嗜酸性粒细胞炎症。用苯乙哌啶（PE）收缩动脉环。在从OVA/盐水和OVA/OVA兔分离的内皮完整的动脉中，与从对照分离的动脉相比，PE反应性增强。一氧化氮合酶（NOS）激动剂NG-硝基-L-精氨酸甲酯（NG-nitro-L-arginine methyl ester）在所有三个实验组中以相似的程度增加对PE的收缩反应，这表明在OVA/盐水和OVA/OVA兔中，NOS活性的降低不参与PE反应的增强。去除内皮后，OVA/盐水和对照兔的动脉显示出相似的PE反应性，表明PE反应性的增强是内皮依赖性的，可能是由于内皮收缩因子。在OVA/OVA兔中，与其他两组相比，内皮剥脱的动脉显示出降低的PE反应性;这种差异被NG-硝基-L-精氨酸甲酯消除。我们的结论是，与OVA本身的全身致敏增强PE诱导的收缩的孤立的支气管动脉在兔的内皮依赖性机制和过敏性肺部炎症减弱这种影响，增加非内皮NOS活性。
We tested the hypothesis that atopy and/or allergic lung inflammation enhances α1-adrenoceptor-mediated contractions of the bronchial artery. Bronchial arterial resistance vessels were isolated from rabbits that had undergone either systemic ovalbumin (OVA) sensitization followed by saline aerosol challenge (OVA/saline rabbits), or OVA sensitization followed by OVA aerosol challenge (OVA/OVA rabbits), or no sensitization followed by saline aerosol challenge (control rabbits). In OVA/OVA rabbits, bronchoalveolar lavage and lung histology revealed lymphocytic and eosinophilic inflammation. Arterial rings were contracted with phenylephrine (PE). In endothelium-intact arteries isolated from OVA/saline and OVA/OVA rabbits, PE responsiveness was enhanced compared with that of arteries isolated from controls. The nitric oxide synthase (NOS) inhibitorNG-nitro-l-arginine methyl ester increased the contractile response to PE in all three experimental groups to a similar degree, suggesting that depressed NOS activity was not involved in the enhanced PE responsiveness in OVA/saline and OVA/OVA rabbits. After endothelium removal, arteries from OVA/saline and control rabbits showed similar PE responsiveness, indicating that the enhancement of PE responsiveness was endothelium dependent, possibly due to an endothelial constricting factor. In OVA/OVA rabbits, endothelium-denuded arteries showed decreased PE responsiveness compared with the other two groups; this difference was abolished byNG-nitro-l-arginine methyl ester. We conclude that systemic sensitization with OVA per se enhances PE-induced contractions of isolated bronchial arteries in rabbits by an endothelium-dependent mechanism and that allergic lung inflammation attenuates this effect by increased nonendothelial NOS activity.