• S Shimura, T Sasaki, H Ishihara, M Satoh, T Masuda, H Sasaki, and T Takishima.
• First Department of Internal Medicine, Tohoku University School of Medicine, Sensai, Japan.
• Nihon Kyobu Shikkan Gakkai Zasshi. 1990 Oct 1;28(10):1299-304.

AbstractA large amount of mucus and mucoid impaction are observed in the autopsied lungs of bronchial asthmatics. It is possible that mucus hypersecretion and accumulation of intrabronchial mucus result in bronchial obstruction and structural bronchial hyperresponsiveness. Bronchial gland plays a main role in human airway secretion. We describe here some results using isolated gland preparation which enable us to examine airway mucus secretion in a well-defined condition. Chemical mediators released from mast cells augment the secretory responses induced by cholinergic nerve stimulation through accelerated acetylcholine release in the nerve terminals. PAF produces an increase in mucus glycoprotein secretion in the presence of platelets mainly through the thromboxane release from platelets. Substance P which is released by an axon reflex in response to various stimuli and inflammations in the airways, also produced an increase in mucus secretion. Epithelial cells release an inhibitory factor to mucus glycoprotein secretion from bronchial glands. Epithelial cell damages due to inflammation in the airways may induced a reduction of the inhibitory factor release in bronchial asthmatics, resulting in mucus hypersecretion.

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