摘要
目的:研究气道速激肽在卵蛋白致敏和激发豚鼠咳嗽发生机制中的作用。方法:正常和卵蛋白致敏豚鼠各20只,卵蛋白雾化吸入激发。24h后,正常组和致敏组豚鼠随机各分为2组,每组10只,分别依次腹腔注射生理盐水,0.1mg/kg、0.3mg/kg和1.0mg/kg的NK1受体拮抗剂SR140333或NK2受体拮抗剂SR48968,观察吸入10-4mol/L的辣椒素溶液诱导的咳嗽反应。用非侵入性方法测量正常和卵蛋白致敏豚鼠注射SR140333或SR48968前后吸入辣椒素溶液所产生的特异性气道阻力。结果:致敏豚鼠咳嗽反应明显高于正常对照组[(9.3±1.2)times/3minvs(19.5±5.7)times/3min,P<0.05]。SR140333不影响正常对照组豚鼠的咳嗽反应,而SR48968则可降低咳嗽频率达30%(P<0.05),两者均抑制吸入辣椒素后增加的气道阻力。而在卵蛋白致敏豚鼠,SR140333或SR48968均抑制吸入辣椒素溶液诱导的咳嗽频率[(9.9±4.7)times/3min,(8.0±1.6)times/3min,P<0.05]和增高的气道阻力。结论:NK受体拮抗剂抑制致敏豚鼠卵蛋白激发后增高的咳嗽反应。因此,气道速激肽可能是嗜酸性粒细胞性气道炎症所致咳嗽的重要介质。
AIM： To investigate the role of tachykinin in airway in cough response in guinea pigs sensitized and challenged with ovalbumin. METHODS： 20 normal and 20 sensitized guinea pigs were challenged with the aerosol of ovalbumin, twen- ty - four hours later, cough response to inhaled capsaicin was measured after the normal and sensitized guinea pigs （ 10 of each） in- troperitoneally injected either with 0.1 mg/kg, 0.3 mg/kg and 1.0 mg/kg of NK1 antagonist SR140333 or NK2 antagonist SR48968, respectively. Specific airway resistance was recorded with noninvasive technique. ~TS： Cough response increased in sensitized guinea pigs compared with control [（ 19.5 ± 5.7） times/3 min vs （9.3 ± 1.2） times/3 min, P 〈 0.053. SR48968FR decreased the cough response by 30% in control guinea pigs （ P 〈 0.05）, but SR140333 did not. Both prevented an increase in airway resistance after the inhalation of capsaicin. However, SR48968FR and SRI140333 inhibited increased cough response [ （9.9±4.7） times/3 min, （8.0±1.6） times/3 min, P 〈 0.05 ] and airway resistance induced by the inhalation of capsaicin. CONCLUSION： Neurokinin （NK） antagonist inhibits increased cough response in guinea pigs sensitized and challenged with ovalbumin. Tachykinin may be. an important mediator in cough associated with eosinophilic airway inflammation.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第9期1744-1747,共4页
Chinese Journal of Pathophysiology
