摘要
急性肺损伤是重症急性胰腺炎(SAP)常见的并发症和死亡的重要原因,其病理生理机制尚不明确。目前认为P物质、神经激肽-1受体、环氧合酶-2、细胞粘附分子、胰酶以及白介素-8、-10、肿瘤坏死因子-α、核因子-κB等多种细胞因子均不同程度地参与了SAP并发急性肺损伤的过程。这些炎症介质间的相互作用,以及炎症从局部向全身扩散的机制尚待研究。
Acute pancreatitis associated lung injury （APALI） is one of the most common complications of severe acute pancreatits（SAP）, while its mechanism is still unclear. This review summarizes the current pathophysiological opinions on the development of APALI, and focuses on the roles of substance P, neurokin-1 receptor, cyclooxygenase-2, intercellular adhesion molecule-1, panereatin and several cytokines, including interleukin 8 and 10, tumor necrosis factor-α, and nuclear factor-kB, etc, However, the interaction among those inflammatory factors needs further investigation.
出处
《国际消化病杂志》
CAS
2006年第6期419-422,共4页
International Journal of Digestive Diseases
关键词
重症急性胰腺炎
肺损伤
发病机制
Acute pancreatitis
Lung injury
Pathophysiologyphy
