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缓激肽在豚鼠变应原诱导的气道微血管渗漏和支气管收缩中不起作用。

Lack of a role for bradykinin in allergen-induced airway microvascular leakage and bronchoconstriction in the guinea pig.

作者信息

Sakamoto T, Barnes P J, Chung K F

机构信息

Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.

出版信息

Inflamm Res. 1996 Mar;45(3):123-6. doi: 10.1007/BF02265164.

Abstract

We have investigated the role of bradykinin in allergen-induced airway microvascular leakage and bronchoconstriction in sensitized guinea pigs. We used a selective bradykinin B2 receptor antagonist, HOE140, which has been shown to prevent the airway effects induced by bradykinin. Lung resistance (RL) was measured for 6 min after challenge with allergen. Extravasation of Evans blue dye into airway tissues was used as an index of the airway microvascular leakage. Aerosolized ovalbumin (5 mg/ml, 30 breaths) induced a significant increase in RL and leakage of dye in the trachea, main bronchi and intrapulmonary airways in the ovalbumin-sensitized guinea pigs. HOE140 given by inhalation (200 microM, 60 breaths) had no effect on the airway microvascular leakage and bronchoconstriction induced by the allergen. I.v. HOE140 (200 nmol/kg) did not significantly inhibit these airway responses. We conclude that bradykinin-mediated mechanism may not play a significant role in airway microvascular leakage or bronchoconstriction induced by allergen.

摘要

我们研究了缓激肽在致敏豚鼠变应原诱导的气道微血管渗漏和支气管收缩中的作用。我们使用了一种选择性缓激肽B2受体拮抗剂HOE140,已证明其可预防缓激肽诱导的气道效应。变应原激发后6分钟测量肺阻力(RL)。伊文思蓝染料向气道组织的渗出用作气道微血管渗漏的指标。雾化卵清蛋白(5mg/ml,30次呼吸)可导致卵清蛋白致敏豚鼠的气管、主支气管和肺内气道的RL显著增加以及染料渗漏。吸入HOE140(200μM,60次呼吸)对变应原诱导的气道微血管渗漏和支气管收缩无影响。静脉注射HOE140(200nmol/kg)未显著抑制这些气道反应。我们得出结论,缓激肽介导的机制可能在变应原诱导的气道微血管渗漏或支气管收缩中不发挥重要作用。

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