Kagoshima M, Tomomatsu N, Aratani H, Terasawa M
Research Laboratories, Yoshitomi Pharmaceutical Industries, Fukuoka, Japan.
Int Arch Allergy Appl Immunol. 1991;96(3):238-43. doi: 10.1159/000235501.
Effect of Y-20811 on airway hyperresponsiveness was studied in sensitized guinea pigs. Airway hyperresponsiveness to acetylcholine (ACh) reached maximum 7 h after antigen challenge in guinea pigs sensitized actively. Y-20811 (0.3-3 mg/kg) administered orally 3 h prior to challenge inhibited this airway hyperresponsiveness in a dose-dependent manner. Y-20811 (3 mg/kg) administered orally 4 h after antigen challenge also decreased the airway hyperresponsiveness. On the other hand, Y-20811 did not affect the bronchoconstriction induced by ACh, serotonin and histamine in nonsensitized guinea pigs. The number of eosinophils in bronchoalveolar lavage fluid in the guinea pig reached the peak 7 h after antigen challenge. Y-20811 had a tendency to decrease the number of total cells, macrophages and eosinophils in a dose-dependent manner. These results suggest that Y-20811 suppress the asthmatic mechanism which causes antigen-induced airway hyperresponsiveness.
研究了Y-20811对致敏豚鼠气道高反应性的影响。在主动致敏的豚鼠中，抗原激发后7小时，气道对乙酰胆碱（ACh）的高反应性达到最大值。在激发前3小时口服Y-20811（0.3 - 3毫克/千克）以剂量依赖的方式抑制了这种气道高反应性。在抗原激发后4小时口服Y-20811（3毫克/千克）也降低了气道高反应性。另一方面，Y-20811对未致敏豚鼠中由ACh、血清素和组胺诱导的支气管收缩没有影响。豚鼠支气管肺泡灌洗液中的嗜酸性粒细胞数量在抗原激发后7小时达到峰值。Y-20811有以剂量依赖的方式减少总细胞、巨噬细胞和嗜酸性粒细胞数量的趋势。这些结果表明，Y-20811抑制了导致抗原诱导气道高反应性的哮喘机制。
