肥大细胞在非过敏性阻塞性肺病理中支气管收缩中的作用。

N A Kuzubova, A N Fedin, E S Lebedeva, O N Titova
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引用次数: 0

摘要

在大鼠慢性阻塞性肺疾病60天间歇性暴露二氧化氮模型中,肥大细胞参与支气管平滑肌收缩活动模式的机制进行了评估。从第31天开始,一组大鼠每天在二氧化氮暴露前吸入甘糖酸钠以稳定肥大细胞膜。另一组(对照组)未接受治疗。测定了支气管分离制剂在神经或平滑肌刺激下的等距收缩。通过稳定细胞膜抑制肥大细胞脱颗粒和内源性组胺的释放,可防止长时间吸入二氧化氮引起的支气管平滑肌过度活跃。我们认为,增加支气管壁平滑肌收缩活性的机制是通过激活常驻肥大细胞中的跨膜腺苷受体介导的,导致其部分脱颗粒,释放组胺,通过壁内神经节神经元启动反射通路,作用于组胺hl受体。
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[ROLE OF MAST CELLS IN BRONCHIAL CONTRACTION IN NONALLERGIC OBSTRUCTIVE LUNG PATHOLOGY].

In model of chronic obstructive pulmonary disease induced in rats by 60-day intermittent exposure to nitrogen dioxide mast cells participation in the mechanism of bronchial smooth muscle contractile activity patterns was evaluated. Since the 31st day, one group of rats was inhaled with sodium cromoglycate every day before the nitrogen dioxide exposure to stabilize the mast cell membrane. The other group (control) hasn’t been treated. Isometric contraction of the bronchial isolated preparations in response to nerve or smooth muscle stimulation were determined. Inhibition of mast cell degranulation and the release of endogenous histamine by stabilizing cell membranes prevented the development of bronchial smooth muscle hyperactivity caused by prolonged inhalation of nitrogen dioxide. It is believed that a mechanism to increase the contractile activity of the bronchial wall smooth muscles is mediated by activation of the transmembrane adenosine receptor in resident mast cells, leading to their partial degranulation with release of histamine, acting on the histamine Hl-receptors with the launch of reflex pathways through intramural ganglion neurons.

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