Involvement of neurogenic inflammation in antigen-induced bronchoconstriction in guinea pigs.
Involvement of neurogenic inflammation in antigen-induced bronchoconstriction in guinea pigs.
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神经源性炎症参与豚鼠抗原诱导的支气管收缩。
DOI：
10.1152/ajplung.1993.265.5.l507
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Nadel,JA
中科院分区：
文献类型：
--
作者：
Bertrand,C;Geppetti,P;Graf,PD;Foresi,A;Nadel,JA
在戊巴比妥钠麻醉、阿托品预处理的致敏豚鼠上，研究了感觉神经释放的速激肽在抗原引起的支气管收缩中的作用。NK 2（SR-48968）和NK 1（CP-96，345）速激肽受体拮抗剂的组合消除了由静脉内辣椒素引起的总肺阻力（RL）的增加，但不影响由静脉内组胺引起的反应。小剂量的雾化卵清蛋白（OVA，0.1%）产生了一个小的增加RL进一步增加，并显着延长中性内肽酶（NEP）抑制剂phosphoramidon;这支气管收缩作用的OVA显着减少的NK 2受体拮抗剂和废除的NK 1和NK 2受体拮抗剂的组合在一起。当使用较大剂量的OVA（0.5%）时，获得最大支气管收缩反应。Phosphoramidon没有显著增强这种反应。NK 1-和NK 2-受体拮抗剂的组合在5分钟时仅轻微地减弱反应，但明显地减弱后来（10-20分钟）的反应。这些结果表明，从感觉神经释放的速激肽在抗原诱导的豚鼠支气管收缩中起重要作用。当NEP对神经肽的正常调节被抑制时，这种作用被夸大，并且主要由NK 2受体活化介导，NK 1受体的贡献较小。
The role of tachykinins released from sensory nerves in bronchoconstriction induced by antigen was studied in sensitized guinea pigs anesthetized with pentobarbital sodium and pretreated with atropine. The combination of NK2 (SR-48968) and NK1 (CP-96,345) tachykinin-receptor antagonists abolished the increase in total pulmonary resistance (RL) evoked by intravenous capsaicin but did not affect the response evoked by intravenous histamine. A small dose of aerosolized ovalbumin (OVA, 0.1%) produced a small increase in RL that was further increased and markedly prolonged by the neutral endopeptidase (NEP) inhibitor phosphoramidon; this bronchoconstrictor effect of OVA was markedly reduced by the NK2-receptor antagonist and was abolished by the combination of the NK1 and NK2-receptor antagonists together. When a larger dose of OVA (0.5%) was used, a maximal bronchoconstrictor response was obtained. Phosphoramidon did not potentiate this response significantly. The combination of NK1- and NK2-receptor antagonists blunted the response at 5 min only slightly but markedly attenuated the later (10–20 min) response. These results show that tachykinins released from sensory nerves play a significant role in antigen-induced bronchoconstriction in guinea pigs. This effect is exaggerated when the normal modulation of neuropeptides by NEP is inhibited and is mediated predominantly by NK2-receptor activation, with a smaller contribution by NK1 receptors.