抽象
速激肽,如P物质,可能参与了气道高反应(AHR)和气道炎症的发展。但是,目前还不清楚其中速激肽受体介导这些生物的活动。速激肽神经激肽-1(NK 1)的2拮抗剂和速激肽神经激肽-2(NK 2)受体,SR 140333和SR 48968的影响,分别在P物质(SP)诱发的气道高反应和的组胺诱导的增强研究增加微血管渗漏,在磷酸阿米酮预处理豚鼠。豚鼠用磷酸阿米酮(0.1mM的气溶胶15分钟)预处理的和单独的或含有SP(0.1 mg.mL-1,30分钟)的盐水溶液暴露15分钟后,以盐溶液。二十四小时后,将动物麻醉并为肺充气压力(PIP)对乙酰胆碱或微血管泄漏到组胺的调查记录制备。Pretreatment of the guinea-pigs with a single dose of SR 48968 (1 mg.kg-1, i.p.) 30 min before SP exposure, significantly prevented the development of AHR, whereas SR 140333 (1 mg.kg-1, i.p.) did not. In a second set of experiments, phosphoramidon-pretreated guinea-pigs exposed to SP presented a significant potentiation of the histamine-induced increase in microvascular leakage in pulmonary airways. When the guinea-pigs were pretreated with SR 140333, an inhibition of the increased microvascular leakage to histamine was observed. In contrast, no significant inhibitory activity was noted when the guinea-pigs were pretreated with SR 48968. The present data demonstrate the importance of tachykinin NK2 receptor stimulation in the development of airway hyperresponsiveness and that of tachykinin NK1 receptor stimulation in microvascular leakage hypersensitivity in phosphoramidon-pretreated and substance P-exposed guinea-pigs. The results also suggest a dissociation between the presence of microvascular leakage and the occurrence of airway hyperresponsiveness.