Estimate of the subepithelial hydrostatic pressure that drives inflammatory transudate into the airway lumen.
Estimate of the subepithelial hydrostatic pressure that drives inflammatory transudate into the airway lumen.
复制标题
估计将炎症渗出液推入气道腔的上皮下静水压。
DOI：
10.1152/japplphysiol.00645.2001
复制
发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Widdicombe,JH
中科院分区：
文献类型：
--
作者：
Serikov,VB;Jang,YJ;Widdicombe,JH
上呼吸道的炎性疾病的特征在于血浆滤液穿过上皮流入气道腔（“渗出”）。在其他地方，我们提出微血管外渗引起水肿，这与上皮下静水压力升高有关，从而导致渗出。为了验证这一假设，我们试图通过提高管腔静水压力来阻断漏出。我们测量了血浆标记物进入大鼠气管在体内的一个孤立的灌注段的管腔中的外观，发现刺激一条迷走神经引起标记物从血液到气道管腔的流动的快速（半衰期<5 min）和非选择性增加。白细胞迁移也引起渗出，其发展缓慢得多（半衰期= 2-3小时）。在这两种情况下，通过应用管腔静水压力来阻断漏出。阻断迷走神经诱导的渗出所需的临界管腔压力为1.45 cmH 2 O，阻断白细胞运输诱导的上皮渗出所需的临界管腔压力为3 cmH 2 O，我们得出结论，这些是驱动炎性渗出进入气道管腔的上皮下压力。
Inflammatory diseases of the upper respiratory tract are characterized by flow of plasma filtrate across the epithelium into the airway lumen (“transudation”). Elsewhere, we have proposed that extravasation from microvessels causes edema, and this is associated with elevated subepithelial hydrostatic pressure that drives transudation. To test this hypothesis, we have attempted to block transudation by elevating luminal hydrostatic pressure. We measured the appearance of plasma markers into the lumen of an isolated perfused segment of rat trachea in vivo and found that stimulation of one vagal nerve caused a rapid (half-time ∼5 min) and nonselective increase in the flow of markers from blood to airway lumen. Leukocyte migration also caused transudation that developed much more slowly (half-time = 2–3 h). In both cases, transudation was blocked by application of luminal hydrostatic pressures. The critical luminal pressure needed to block vagally induced transudation was ∼4.5 cmH2O, and, to block epithelial transudation induced by leukocyte traffic, it was 3 cmH2O, and we conclude that these are the subepithelial pressures that drive inflammatory transudation into the airway lumen.