Ang C, Clark E, Young I, Owe-Young R, Eyland A, Hunt J, Chesterman C, Krilis S
School of Medicine, St. George Hospital, University of New South Wales, Australia.
J Lipid Mediat. 1990 Sep-Oct;2(5):263-9.
Arachidonate metabolism in bronchial mucosa was investigated. Bronchial biopsies from four asthmatics and three non-asthmatic controls were challenged with 300, 465, 650 and 960 mOsm/kg saline in the presence of [3H]arachidonate. Supernatants were analysed by reverse-phase high-performance liquid chromatography. The major arachidonate metabolite was identified as 15-monohydroxyeicosatetraenoic acid (15-HETE), with significantly higher production in biopsies from asthmatics than controls. Statistical analysis of the full model explained 81% of the variation (F = 14.8; df = 6, 21; P less than 0.001). Hyperosmolarity and the presence of sarcoid had no significant effect on 15-HETE synthesis, reducing R2 by only 6%.
对支气管黏膜中的花生四烯酸代谢进行了研究。在存在[3H]花生四烯酸的情况下,用300、465、650和960 mOsm/kg盐水对4名哮喘患者和3名非哮喘对照者的支气管活检组织进行刺激。通过反相高效液相色谱法分析上清液。主要的花生四烯酸代谢产物被鉴定为15-单羟基二十碳四烯酸(15-HETE),哮喘患者活检组织中的生成量显著高于对照者。完整模型的统计分析解释了81%的变异(F = 14.8;自由度 = 6, 21;P小于0.001)。高渗性和结节病的存在对15-HETE合成无显著影响,仅使R2降低6%。