BURNS, TRAUMA AND GUT ORIGIN SEPSIS

烧伤、创伤和肠道源性脓毒症

• 批准号: 6386594
• 负责人: EDWIN A DEITCH
• 金额: $ 43.59万
• 依托单位: UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-09-01 至 2003-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6386594
• 关键词: burns; cytokine; disease /disorder etiology; gut associated lymphoid tissue; hemorrhagic shock; immunomodulators; laboratory rat; lung injury; lymph; mesentery; microcirculation; multiple organ failure; neutrophil; respiratory epithelium; selectins; septic shock; trauma; vascular endothelium permeability

DESCRIPTION (adapted from applicant's abstract): The investigators hypothesize that following shock from either hemorrhage or thermal injury; there is a release of mediators from the gastrointestinal tract, which interact with mesenteric lymphatic system to cause the release of cytotoxic mediators from the mesenteric lymph nodes. The materials from the lymph nodes activate of pulmonary endothelium resulting in the adherence of leukocytes to the pulmonary microvasculature, and pulmonary vascular injury. In their first specific aim the investigators will characterize the action of shock lymph on endothelial cells and neutrophils and identify the humoral factors present in the mesenteric lymph after injury. The second specific aim they will determine the role of adherence molecule expression on the shock induced lung injury. The final specific aim will determine mechanisms by which mesenteric lymph from blood or burned rats, produces the lung injury. They will determine how diversion of the lymphatic drainage from the gut will prevent the pulmonary changes (deposition of cells in the lung, expression of adherence molecules and cytokines) associated with hypovolemic and burn shock. They will inject lymph into the animals and evaluate changes in the lung. This work will help to determine why disruption of gut barrier function will lead to lung injury. It will also more clearly define the role of the gut inducing lung injury and in the development of the systemic inflammatory response syndrome and multiple organ failure (MOF).

描述(改编自申请者摘要)：调查人员假设 在失血或热损伤引起的休克后，有一个 从胃肠道释放介质，与之相互作用 肠系膜淋巴系统导致细胞毒介质从 肠系膜淋巴结。来自淋巴结的物质激活了 肺内皮细胞导致白细胞与肺的黏附 微血管和肺血管损伤。在他们的第一个具体目标 研究人员将确定休克淋巴对内皮细胞的作用 细胞和中性粒细胞，并确定存在于 损伤后肠系膜淋巴。他们将确定的第二个具体目标 黏附分子表达在休克肺损伤中的作用这个 最终的特定目标将决定肠系膜淋巴从 血或烧伤的大鼠，会产生肺损伤。他们将决定如何 肠道淋巴引流的分流将防止肺脏 变化(肺内细胞沉积、黏附分子表达和 细胞因子)与低血容量和烧伤休克有关。他们会注射淋巴 注入动物体内，评估肺部的变化。这项工作将有助于 确定为什么肠道屏障功能障碍会导致肺损伤。它 也将更清楚地定义肠道导致肺损伤和在 全身炎症反应综合征与多发性硬化的研究进展 器官衰竭(MOF)。