电毁损鼠下丘脑前区致急性肺水肿的实验研究

A Study on Fulminating Pulmonary Edema after Bilateral Electrolytic Lesion of An- terior Hypothalamus

目的:通过立体定向仪电毁损鼠下丘脑前区(AH),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AH后,分别于0.5、1、2、3 h,测定血、脑组织儿茶酚胺(CA)的含量,毁损AH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AH后血压0.5 h迅速上升到最大值,1 h后逐渐下降。毁损后血CA迅速上升,到1 h上升到最大值,以后逐渐恢复。而毁损后0.5 h脑组织中CA降到最低值,而后迅速恢复。光镜、电镜观察发现电毁损AH 1 h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:AH是引起NPE的主要结构,其结构和功能的破坏是引起NPE的根本基础。

Objective: To study the centrum mechanism of the neurogenic pulmonary edema (NPE) by the stereotactic electrolytic injury to the bilateral Anterior hypothalamus (AH) in medulla of rats. Methods: We used the stereolytic electrolytic injury to destroy the bilateral AH in medulla of SD rats, then mensurated the changes of catecholamine in the serum and brain tissue in 0. 5, 1,2, 3 hour respectively, and the changes of blood pressure in 3 hours, as well as the pulmonary pathology observed by the electro-microscope and microscope. Results: Thirty minutes after stereotactic electrolytic injury BP jumped to maximum quickly and maintain 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 down to minimum after 0. 5 hour, recovered dramatically. The pathological examination demonstrated the lungs capillary hyperemia with alveolar and interstitial edema and infiltration of inflammatory cells. Conclusion: AH which is the core of modulating sympathetic nerve plays an important role in the course of NPE. Dysfunction of it is the basis of NPE.