TRACHEOBRONCHIAL LESIONS OF INHALATION INJURY

吸入烟雾会导致严重的肺部问题。 这大大增加了患者的发病率和死亡率 皮肤灼伤。这项建议将在 烟雾吸入致绵羊慢性充血模型的建立 和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肠道。 这些介质包括血栓素A2、组胺、白三烯 和氧自由基。结合从细胞中脱落的细胞 在呼吸道内，这种渗出物形成投射在 导致严重呼吸道阻塞的气管、支气管树。电浆 上部释放的蛋白质和炎症介质 呼吸道刺激巨噬细胞产生和释放 趋化物质导致多形核白细胞 分泌和释放蛋白水解酶和自由基 伴有纤毛直接破坏的间质 上皮细胞和粘液产生细胞。血浆和血液样本 淋巴将从隔离的气管和双侧气管收集 吸入烟雾前后的单侧肺模型 受伤。这些将被分析为炎症介质 在受伤现场被释放。局部和系统的调节 气管、支气管炎性介质可能改变 进行性肺功能障碍与高死亡率 以严重的烟雾吸入性损伤为特征。

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.