Permeability of intraneural microvessels and perineurium following acute, graded experimental nerve compression.

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.