BURNS, TRAUMA AND GUT ORIGIN SEPSIS

烧伤、创伤和肠道源性脓毒症

• 批准号: 6781641
• 负责人: EDWIN A DEITCH
• 金额: $ 12.74万
• 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 2004-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6781641
• 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（改编自申请人摘要）：研究者假设