Effects of inflammatory and other mediators on airway vascular beds.

Effects of inflammatory and other mediators on airway vascular beds.
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炎症和其他介质对气道血管床的影响。

DOI:
10.1164/arrd.1987.135.6p2.s67
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发表时间:
2015
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
J. Widdicombe
J. Widdicombe
中科院分区:
--
文献类型:
--
作者:
L. Laitinen;A. Laitinen;J. Widdicombe

文献摘要

被引文献

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支气管动脉延伸至除肺泡壁外的所有肺结构。除了为肺部提供营养外,支气管血管还可以作为血液动力学和气体交换系统发挥作用,这是由于支气管血管与肺动脉的相互作用;支气管血管还在控制化学介质的清除、调节气道壁水肿的发展以及控制气管支气管树中的热交换方面发挥重要作用。我们测量了炎症介质和其他介质对犬气管粘膜厚度和气管血管阻力变化的影响。缓激肽、组胺和乙酰甲胆碱具有较大的“血管扩张剂”作用,降低血管阻力,并且它们也明显增加粘膜厚度。P物质、VIP、PGF 2 α和PGE 1对血管阻力的反应与上述药物一样大,但对增加气管粘膜厚度的作用很小。沙丁胺醇的反应模式介于这两组之间。苯乙醯胺有相反的作用,引起血管阻力增加和粘膜厚度减少。尽管血管活性药物导致血管舒张和血管通透性增加,但粘膜厚度的变化相当小,并且与不同药物导致的血管阻力降低无关。这种变化不太可能对气管气道阻力产生明显影响。粘膜厚度的变化在粘膜厚度变化与相邻管腔半径的比率较大的气道部分中可能更显著,例如鼻和小的传导气道。
The bronchial arteries extend to all lung structures in man with the exception only of the alveolar wall. In addition to providing nutrition to the lungs, the bronchial vessels can also function as a hemodynamic and gas-exchange system due to anastomoses with the pulmonary arteries; they also play a significant role in controlling the clearance of chemical mediators, regulating the development of airway wall edema, and controlling heat exchange in the tracheobronchial tree. We have measured the effects of inflammatory and other mediators on tracheal mucosal thickness and the changes in tracheal vascular resistance in dogs. Bradykinin, histamine, and methacholine had large "vasodilator" effects, decreasing vascular resistance, and they also clearly increased the thickness of the mucosa. Substance P, VIP, PGF2 alpha, and PGE1 had as large a response on vascular resistance as the drugs mentioned above, but only had small effects in increasing tracheal mucosal thickness. Salbutamol fell between these 2 groups with regard to the pattern of response. Phenylephrine had an opposite action, causing an increase in vascular resistance and a decrease in mucosal thickness. Despite the vasodilatation and the increase in vascular permeability due to vasoactive drugs, the changes in mucosal thickness were rather small and could not be correlated with the decreases in vascular resistance due to the different drugs. Such changes are unlikely to have an appreciable effect on tracheal airway resistance. The change in mucosal thickness may be more significant in those parts of the airways where the ratio of change in mucosal thickness to the radius of adjacent lumen is large, such as the nose and small conducting airways.