TRACHEOBRONCHIAL LESIONS OF INHALATION INJURY

吸入烟雾会引起严重的肺部问题 这大大增加了患者的发病率和死亡率 皮肤烧伤 该提案将在 慢性烟雾吸入致绵羊充血模型 以及上呼吸道微血管通透性的变化 产生富含炎症介质的渗出物的管道。 这些介质包括血栓素A2、组胺、白三烯 和氧自由基。 结合脱落的细胞 在气道内，这种渗出物在 气管支气管树导致严重的气道阻塞。 血浆 蛋白质和炎症介质释放在上 气道刺激巨噬细胞产生和释放 趋化物质导致多形核白细胞， 使蛋白水解酶和自由O2自由基边缘化， 伴随着纤毛的直接破坏 上皮和粘液产生细胞。 血浆样本和 将从离体气管和双侧收集淋巴液 烟雾吸入前后的单侧肺模型 损伤 这些将被分析为炎症介质 在受伤部位释放。 局部和全身调节 气管支气管炎性介质可能改变 进行性肺功能障碍和高死亡率 严重的烟雾吸入性损伤

The inhalation of smoke produces severe pulmonary problems which greatly increase the morbidity and mortality in patients with a cutaneous burn injury. This proposal will demonstrate in the chronic sheep model that smoke inhalation causes hyperemia and microvascular permeability changes in the upper respiratory tract producing an exudate rich in inflammatory mediators. These mediators include thromboxane A2, histamine, leukotrienes and free oxygen radicals. In combination with cells shed from within the airways this exudate forms casts in the tracheobronchial tree causing severe airway obstruction. Plasma proteins and inflammatory mediators released in the upper airways stimulate macrophages to produce and release chemotactic substances causing polymorphonuclear leukocytes to marginate and release proteolytic enzymes and free 02 radicals in the interstitium with a concomitant direct destruction of ciliated epithelial and mucous producing cells. Samples of plasma and lymph will be collected from isolated trachea and from bilateral and unilateral lung models before and following smoke inhalation injury. These will be analyzed for inflammatory mediators released at the injury site. Topical and systemic modulation of tracheobronchial inflammatory mediators may alter the progressive pulmonary dysfunction and high mortality characteristic of severe smoke inhalation injury.