Bradykinin induces eosinophil accumulation in the rat pleural cavity.

C P Pasquale, M A Martins, P T Bozza, P M Silva, H C Faria Neto, A L Pires, R S Cordeiro
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引用次数: 21

Abstract

Intrathoracic injections of bradykinin (1-100 micrograms/cavity) induced a dose-dependent increase in the number of eosinophils recovered from the rat pleural cavity 24 h later. Eosinophilia by bradykinin was preceded by a marked pleural neutrophil influx within 6 h and was absent only 72 h following stimulation. Bradykinin (10(-9)-10(-5) M) failed to induce in vitro eosinophil chemotaxis, indicating that its in vivo effect must be mediated by an intermediate messenger. BW 755C (25 mg/kg) and the more selective lipoxygenase inhibitor BW A4C (20 micrograms/cavity) suppressed the pleural eosinophilia induced by bradykinin (50 micrograms/cavity), whereas the platelet-activating factor (PAF)-acether antagonist BN 52021 was inactive. We conclude that bradykinin is able to attract eosinophil in vivo by a mechanism independent of PAF-acether and sensitive to the blockage of the lipoxygenase pathway.

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缓激肽诱导大鼠胸膜腔内嗜酸性粒细胞积聚。
胸内注射缓激肽(1-100微克/腔)可诱导24小时后从大鼠胸膜腔中恢复的嗜酸性粒细胞数量呈剂量依赖性增加。缓激肽引起的嗜酸性粒细胞增多在6小时内出现明显的胸膜中性粒细胞内流,刺激后仅72小时消失。缓激素(10(-9)-10(-5)M)未能诱导体外嗜酸性粒细胞趋化,表明其体内作用必须通过中间信使介导。BW 755C (25 mg/kg)和更具选择性的脂氧合酶抑制剂BW A4C(20微克/腔)抑制缓激肽(50微克/腔)诱导的胸膜嗜酸性粒细胞增多,而血小板活化因子(PAF)-醚拮抗剂BN 52021则无活性。我们得出结论,缓激肽能够通过一种独立于paf -醚的机制在体内吸引嗜酸性粒细胞,并且对脂氧合酶途径的阻断敏感。
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