Rydevik B, Lundborg G
Scand J Plast Reconstr Surg. 1977;11(3):179-87. doi: 10.3109/02844317709025516.
Experimental compression lesions of peripheral nerves were induced by applying pressure direct to exposed rabbit nerve trunks. A specifically designed compression chamber was used, enabling application of graded pressures (50--600 mmHg) to the nerves for various periods of time (15 min to 6 hours). After releasing the pressure, analyses were performed concerning the intraneural microvascular permeability and the barrier function of the perineurium. The method used was fluorescence microscopic tracing of intravenously injected or locally applied albumin labelled with Evans blue. The results indicate that a slight trauma to a nerve (e.g. 50 mmHg during 2 hours) induced an epineurial oedema by increasing the permeability of the epineurial vessels, which were more susceptible to compression trauma than the endoneurial vessels. Compression at higher pressure levels or of prolonged duration caused injury also to the endoneurial vessels, leading to intrafascicular oedema formation, which generally was most prominent at the edges of the compressed nerve segment. The perineurial barrier was remarkably resistant to compression trauma. Possible pathophysiological effects of various degrees of post-traumatic intraneural oedema formation are discussed.
通过直接对暴露的兔神经干施加压力来诱导周围神经的实验性压迫损伤。使用了专门设计的压迫室，能够在不同时间段（15分钟至6小时）对神经施加分级压力（50 - 600 mmHg）。释放压力后，对神经内微血管通透性和神经束膜的屏障功能进行了分析。所采用的方法是通过荧光显微镜追踪静脉注射或局部应用的用伊文思蓝标记的白蛋白。结果表明，对神经的轻微创伤（例如2小时内50 mmHg）通过增加神经外膜血管的通透性诱导了神经外膜水肿，神经外膜血管比神经内膜血管更容易受到压迫创伤。更高压力水平或更长时间的压迫也会导致神经内膜血管损伤，从而导致束内水肿形成，这种水肿通常在受压神经段的边缘最为明显。神经束膜屏障对压迫创伤具有显著的抵抗力。讨论了不同程度创伤后神经内水肿形成可能的病理生理效应。
