神经源性肺水肿(NPE)是颅脑创伤、脑血管病变、高原缺氧等常见的并发症,发病急剧凶险.在我国没有引起临床与基础应有的重视。我们用大量注射肾上腺素造成致死性肺水肿,病理过程与NPE+分相似,而程度上更剧烈,具有动力性与非动力性双重机制,既有肺毛细血管流体静压增高,又有毛细血管通透性增高.用山莨菪碱与川芎嗪进行预防,绝大部份动物不形成肺水肿并长期存活,效果明显. Neurogenic pulmonary edema (NPE) is a common complication of craniocerebral trauma, cerebrovascular disease and plateau hypoxia, and its incidence is drastic and dangerous, which has not caused much attention in our country. We use a large number of injection of epinephrine cause fatal pulmonary edema, and NPE + pathological process similar to the degree of more intense, with dynamic and non-motor dual mechanisms, both pulmonary capillary hydrostatic pressure, and capillary access Permeability increased with anisodamine and ligustrazine prevention, most of the animals do not form pulmonary edema and long-term survival, the effect is obvious.