Roquefeuil B
Ann Anesthesiol Fr. 1975;16 Spec No 2-3:51-6.
Neurogenic edema, in the strict sense of the term, has at the present time practically not benefitted from precise hemodynamic investigations in human clinical practice, and owing to this fact, authors still classify them under the heading "mixed edema or of unknown pathogenesis". In contrast with this lack of information in man, animal experimental works are surprising by their coherence and the experimental facility of producing neurogenic edema (cranial hypertension by a small inflatable balloon and cisternal infection of fibrin). If one excludes the now ancient vagal theories (CAMERON 1949; CAMPBELL, 1949) which were never confirmed, all of the most recent experimental works (SARNOFF, 1952; DUCKER, 1968; LUISADA, 1967; MORITZ, 1974) confirm the adrenergic disorder of central origin during neurogenic A.P.E. which from the hemodynamic standpoint is like an authentic hemodynamic A.P.E. with raised left atrial pressure, pulmonary venous pressure and pulmonary capillary pressure.
严格意义上的神经源性水肿，目前在人类临床实践中实际上并未从精确的血流动力学研究中受益，因此，作者们仍将其归类于“混合性水肿或发病机制不明的水肿”这一标题下。与人类缺乏这方面信息形成对比的是，动物实验研究在产生神经源性水肿（通过小的可充气气球造成颅内高压和向脑池注入纤维蛋白）方面的连贯性和实验便利性令人惊讶。如果排除那些从未得到证实的古老迷走神经理论（卡梅伦，1949年；坎贝尔，1949年），所有最新的实验研究（萨诺夫，1952年；达克，1968年；路易萨达，1967年；莫里茨，1974年）都证实了神经源性急性肺水肿期间中枢起源的肾上腺素能紊乱，从血流动力学角度来看，这类似于真正伴有左心房压力、肺静脉压力和肺毛细血管压力升高的血流动力学急性肺水肿。
