Ozone increases susceptibility to antigen inhalation in allergic dogs.
Ozone increases susceptibility to antigen inhalation in allergic dogs.
复制标题
臭氧会增加过敏犬对抗原吸入的敏感性。
DOI：
10.1152/jappl.1990.68.6.2267
复制
发表时间：
1990
影响因子：
3.3
通讯作者：
T. Takishima
中科院分区：
文献类型：
--
作者：
M. Yanai;T. Ohrui;T. Aikawa;H. Okayama;K. Sekizawa;K. Maeyama;Hiroshi Sasaki;T. Takishima
为了确定 O3 暴露是否会增加气道对抗原吸入的反应性，我们研究了对 AA 敏感和不敏感的狗在 O3 之前和之后对乙酰胆碱 (ACh) 和猪蛔虫抗原 (AA) 的气道反应性。通过测定使呼吸阻力 (Rrs) 增加至基线值两倍的 ACh 和 AA 气溶胶的激发浓度来评估气道反应性。 O3（百万分之三）可增加对 AA 敏感和不敏感的狗的气道对 ACh 的反应性，并且显着降低 ACh 激发浓度，从 0.541 +/- 0.095 至 0.102 +/- 0.047 (SE) mg/ml（P 小于 0.01；n = 10）。 AA 气雾剂，即使与 O3 组合达到最高浓度，也不会增加对 AA 不敏感的狗的 Rrs。然而，O3 增加了 AA 敏感犬的气道对 AA 的反应性，并显着降低了对数 AA 激发浓度，从 2.34 +/- 0.22 降至 0.50 +/- 0.17 (SE) 对数蛋白氮单位/ml（P 小于 0.01；n = 7）。 O3 诱导的对 ACh 的高反应性在 2 周内恢复到基线水平，但对 AA 的高反应性持续超过 2 周。 AA激发后血浆组胺浓度明显高于O3前（P小于0.01）。静脉滴注血栓素合成抑制剂OKY-046（100微克.kg-1.min-1）可抑制O3诱导的ACh反应性增加，但对O3诱导的AA反应性增加和血浆组胺浓度增加没有影响。这些结果表明，O3 通过与 O3 诱导的毒蕈碱高反应不同的机制增加致敏狗对抗原的敏感性。
To determine whether O3 exposure increased airway responsiveness to antigen inhalation, we studied airway responsiveness to acetylcholine (ACh) and Ascaris suum antigen (AA) before and after O3 in dogs both sensitive and insensitive to AA. Airway responsiveness was assessed by determining the provocative concentration of ACh and AA aerosols that increased respiratory resistance (Rrs) to twice the base-line value. O3 (3 parts per million) increased airway responsiveness to ACh in dogs both sensitive and insensitive to AA, and it significantly decreased the ACh provocation concentration from 0.541 +/- 0.095 to 0.102 +/- 0.047 (SE) mg/ml (P less than 0.01; n = 10). AA aerosols, even at the highest concentration in combination with O3, did not increase Rrs in dogs insensitive to AA. However, O3 increased airway responsiveness to AA in AA-sensitive dogs and significantly decreased log AA provocation concentration from 2.34 +/- 0.22 to 0.50 +/- 0.17 (SE) log protein nitrogen units/ml (P less than 0.01; n = 7). O3-induced hyperresponsiveness to ACh returned to the base-line level within 2 wk, but hyperresponsiveness to AA continued for greater than 2 wk. The plasma histamine concentration after AA challenge was significantly higher after than before O3 (P less than 0.01). Intravenous infusion of OKY-046 (100 micrograms.kg-1.min-1), an inhibitor of thromboxane synthesis, inhibited the O3-induced increase in responsiveness to ACh, but it had no effects on the O3-induced increase in responsiveness to AA and the increase in the plasma histamine concentration. These results suggest that O3 increases susceptibility to the antigen in sensitized dogs via a different mechanism from that of O3-induced muscarinic hyperresponsiveness.