电毁损鼠延髓孤束核致急性肺水肿的实验研究  

A study on fulminating pulmonary edema after bilateral electrolytic lesion of neucleus solitary tract

作　　者：吴旻[1] 惠国桢[1] 

机构地区：[1]苏州大学附属第一医院脑外科,215006

出　　处：《江苏医药》2002年第5期338-339,342,T003,共4页Jiangsu Medical Journal

摘　　要：目的　通过立体定向仪电毁损鼠延髓孤束核 (NTS) ,探讨神经源性肺水肿 (NPE)的中枢发生机制。方法　采用立体定向电毁损SD大鼠双侧NTS尾侧后 ,分别于 30、6 0、12 0、180分钟 ,测定血、脑儿茶酚胺 (CA)的含量 ,毁损NTS前后血压的变化 ,光镜、电镜观察肺病理变化。结果　立体定向电毁损鼠NTS后血压 30分钟迅速上升到最大值 ,1小时后逐渐下降。毁损后血CA迅速上升 ,到 1小时上升到最大值 ,以后逐渐恢复。而脑CA毁损后 1小时到最低值 ,而后缓慢恢复。光镜、电镜观察发现电毁损NTS 1小时后肺毛细血管充血、水肿、炎性细胞浸润、肺泡腔内有红细胞。结论　NTS是引起NPE的主要结构 。Objective To study the centrum mechanism of the neurogenic pulmonary edema (NPE) by the stereotactic electrolytic lesion in rats,bilateral neucleus of solitary tract (NST) in medulla.Methods We used the stereotactic electrolytic lesion to destroy the bilateral NST in medulla of SD rats,then mensurated the changes of catecholamine in the serum and brain tissue in 30,60,120,180min respectively,and the changes of blood pressure in 3 hours,as well as the pulmonary pathology observed by both electro-microscope and light microscope.Results 30 minutes after stereotactic electrolytic lesion BP jumped to maximum quickly and maintained at the level in an hour then dropped gradually.CA in serum increased quickly to the maximum in an hour,then dropped gradually.While CA in brain fell to minimum after 1 hours,then recovered gradually.The pathological examination demonstrated the lungs'capillary hyperemia alveolar and interstitial edema,and infiltration of inflammatory cells.Conclusion NTS which are the core of modulating sympathetic nerve play an important role in the course of NPE.Its dysfunction is the basis of NPE.

关 键 词：电毁损 延髓孤束核 急性肺水肿 实验研究 

分 类 号：R541.63[医药卫生—心血管疾病]