Sasaki T, Shimura S, Sasaki H, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
J Appl Physiol (1985). 1989 Feb;66(2):764-70. doi: 10.1152/jappl.1989.66.2.764.
We studied the effect of airway epithelium on mucus secretion by use of an isolated tracheal submucosal gland preparation reported previously (J. Appl. Physiol. 60: 1237-1247, 1986). Mucus glycoconjugate release from submucosal glands of feline trachea was examined using [3H]glucosamine as a mucus precursor. Isolated glands showed significantly higher secretory responses to cholinergic, alpha-, and beta-adrenergic agonists and dibutyryladenosine 3',5'-cyclic monophosphate (average 400% of control) than the conventional tracheal mucosal explants, which contained epithelium and submucosal tissues in addition to submucosal glands (average 160% of control). The addition of isolated epithelium depressed the secretory response of isolated glands to the same level as that of tracheal explants. However, the supernatant from isolated epithelium failed to inhibit secretory responses to methacholine in isolated glands, suggesting that the epithelium-derived inhibitory factor to secretion may be short-lived. Leukotriene D4 antagonist (FPL 55712), cyclooxygenase and/or lipoxygenase inhibitors (indomethacin or BW 755C) caused no significant change in the inhibitory action of epithelium, suggesting that the inhibition is not due to arachidonic acid metabolites. The newly found secretory inhibitory action of epithelium is of particular interest in the pathogenesis of hypersecretion associated with epithelial damage.
我们采用先前报道的离体气管黏膜下腺制备方法(《应用生理学杂志》60: 1237 - 1247, 1986),研究了气道上皮对黏液分泌的影响。以[³H]葡糖胺作为黏液前体,检测猫气管黏膜下腺黏液糖缀合物的释放。与传统的气管黏膜外植体相比,离体腺体对胆碱能、α-和β-肾上腺素能激动剂以及二丁酰腺苷3',5'-环磷酸(平均为对照的400%)表现出显著更高的分泌反应,传统气管黏膜外植体除了黏膜下腺外还包含上皮和黏膜下组织(平均为对照的160%)。添加离体上皮可将离体腺体的分泌反应抑制至与气管外植体相同的水平。然而,离体上皮的上清液未能抑制离体腺体对乙酰甲胆碱的分泌反应,这表明上皮来源的分泌抑制因子可能是短暂存在的。白三烯D4拮抗剂(FPL 55712)、环氧化酶和/或脂氧合酶抑制剂(吲哚美辛或BW 755C)对上皮的抑制作用没有显著影响,这表明该抑制作用并非由花生四烯酸代谢产物引起。上皮新发现的分泌抑制作用在与上皮损伤相关的分泌亢进的发病机制中尤为重要。