Parry G J, Brown M J
J Neurol Sci. 1981 Apr;50(1):123-33. doi: 10.1016/0022-510x(81)90047-2.
Despite the clinical importance of ischemia in the pathogenesis of many human neuropathies, little is known about the effect of circulatory compromise on the structure of peripheral nerves. This results in part from the lack of an entirely satisfactory model in which to study ischemic neuropathy. We therefore injected arachidonic acid, a potent stimulus to platelet aggregation and vasoconstriction, into the femoral artery of normal rats. This resulted in the rapid onset of focal infarction of the proximal posterior tibial nerve in all animals. Distally there was evidence of Wallerian degeneration but not of primary ischemic damage. The site and nature of the infarct and the temporal sequence of the pathological changes were highly consistent. This new method is a simple and highly reproducible means of producing experimental nerve infarction.
尽管缺血在许多人类神经病变的发病机制中具有临床重要性，但关于循环功能受损对周围神经结构的影响却知之甚少。部分原因是缺乏一个完全令人满意的研究缺血性神经病变的模型。因此，我们将花生四烯酸（一种对血小板聚集和血管收缩有强烈刺激作用的物质）注入正常大鼠的股动脉。这导致所有动物的胫后神经近端迅速出现局灶性梗死。在远端有华勒氏变性的证据，但没有原发性缺血损伤的证据。梗死的部位和性质以及病理变化的时间顺序高度一致。这种新方法是产生实验性神经梗死的一种简单且高度可重复的手段。
