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Flexor tendon from the synovial sheath region of rabbits was resected and placed as a free body in a synovial knee joint recess. Structural changes of the surface of the graft caused by the instruments used to handle the tendon during the surgery (jewellers microforceps), was analysed by electron microscopy at various time intervals up to 6 weeks. The superficial coat of amorphous material, i.e. ground substance, on the surface of the tendon was dishevelled by the instruments. The injured areas were crowded with monocytes and macrophages during the first days. An increasing number of fibroblasts and mesothelial-like cells covered the damaged area in less than two weeks. The superficial coat of ground substance was not completely restored until after 3 weeks or more. The results obtained are discussed in relation to functional aspects.

Surgical treatment of peripheral nerve lesions associated with intraneural fibrosis is sometimes extended to include internal neurolysis. This procedure is performed in order to release the individual nerve fascicles from interfascicular scar tissue which is believed to constrict nerve fibres and thereby interfere with their function and regenerative capacity. However, an internal neurolysis per se implies a significant trauma to the nerve and may induce microvascular damage and formation of new intraneural scar tissue. Considering this, such a procedure appears justified only when the preoperative intraneural fibrosis is more severe than the scarring which might be induced by the surgical procedure as such. In order to evaluate the tissue reactions following internal neurolysis an experimental investigation was carried out: internal neurolysis was performed on normal rabbit tibial nerve. After varying postoperative periods up to 6 months specimens of nerves were analysed. Reactive changes of connective tissue and myelin sheath lesions, indicating nerve fibre damage, were investigated in histological sections studied by light microscopy. Barrier function of perineurial membrane and endoneurial vessels was investigated by fluorescent microscopic tracing of locally applied or intravenously injected albumin labelled with Evans' blue. The results indicate that an experimental internal neurolysis per se may induce fibrosis in all layers of the nerve and may cause some nerve fibre damage. However, the barrier function of the perineurium and the endoneurial vessels seems to be generally well preserved. The findings are discussed in relation to indications for internal neurolysis.

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.