摘要
目的 :探讨内皮素 1(ET 1)在神经源性肺水肿 (NPE)发病机理中的作用。方法 :采用Marmarous闭合性颅脑损伤模型致大鼠重度、弥漫性颅脑损伤 ,检测血浆、肺匀浆中ET 1的含量 ,并用免疫组化方法检测肺ET 1的表达。结果 :大鼠重度弥漫性颅脑损伤后 1h起血浆及肺匀浆中ET 1含量增加 ,6h达高峰 ,2 4h以后略有下降 ,但是 ,在4 8h内一直维持在较高水平 (P <0 .0 5 )。病理学检查显示 :伤后 1h起肺毛细血管扩张、充血 ;肺间隔增宽 ,有以中性粒细胞及单个核细胞为主的白细胞浸润 ,6h最明显 ;2 4h、4 8h肺充血、肿胀 ,肺泡腔内充满大量嗜伊红的蛋白渗出物。免疫组化显示 :ET 1在实验组较对照组阳性表达增强 ,光密度值增高 ,以 6h最显著。结论 :ET
Aim: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. Methods: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous'model.The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. Results: After heavy diffuse brain injury in rats,the levels of endothelin-1 in plasma and lung began increasing at 1 hour ,and peaked at 6 hour. Though a little declining at 24 hour,it maintained a higher level within 48 hours (P<0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue,and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion,swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically , endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. Conclusion: The inflammatory injury machanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2004年第3期268-271,共4页
Chinese Journal of Applied Physiology
关键词
内皮素-1
神经源性肺水肿
炎性损伤机制
endothelin-1
neurogenetic pulmonary injury
machenism of inflammatory injury
