Defects of sixteen peripheral nerve were re-paired by skeletal muscle bridging from December1986 though December 1989. Satisfactory resultswere achieved after follow-up for 8-31 months.The key point of this operation were proper explo-ration and exposure of the nerve stumps ,thoroughresection of the cicatricial tissues from the stumpsproper chois of muscular fascicle for bridging, pro-viding a good blood supply to the muscle strip, andcorrect suture of the nerve under microscope. Irri-gation of the operativ field with hydrocortisone could play some roles of decreasing the postoperative local inflammation,edema,adhesion, and scar formation.
OBJECTIVE Following the delayed repair of peripheral nerve injury, the cell number of anterior horn of the spinal cord and its ultrastructural changes, motorneuron and its electrophysiological changes were investigated. METHODS In 16 rabbits the common peroneal nerves of both sides being transected one year later were divided into four groups randomly: the degeneration group and regeneration of 1, 3 and 5 months groups. Another 4 rabbits were used for control. All transected common peroneal nerves underwent epineural suture except for the degeneration group the electrophysiological examination was carried out at 1, 3 and 5 months postoperatively. Retrograde labelling of the anterior horn cells was demonstrated and the cells were observed under light and electronmicroscope. RESULTS 1. The number of labelled anterior horn cell in the spinal cord was 45% of the normal population after denervation for one year (P lt; 0.01). The number of labelled cells increased steadily from 48% to 57% and 68% of normal values at 1, 3 and 5 months following delayed nerve repair (P lt; 0.01). 2. The ultrastructure of the anterior horn cells of the recover gradually after repair. 3. With the progress of regeneration the latency become shortened, the conduction velocity was increased, the amplitude of action potential was increased. CONCLUSION Following delayed repair of injury of peripheral nerve, the morphology of anterior horn cells of spinal cord and electrophysiological display all revealed evidence of regeneration, thus the late repair of injury of peripheral nerve was valid.
Motor endplate is the structure connected between the nerve terminal and muscle fibre and plays a very important role in conducting nerve impulses to the target, therefore, systemical study of the sequential changes of the motor end-plate upon denervation is quite important.Ninety New Zealand rabbits were divided into nine groups from two weeks to nine months after denervation. Acetycholinesterase(AchE) was analyzed quantitatively to study the sequential changes of the motorendplates of tibialis anterior muscle. The results showed that there was no significant reduction of AchE at theend if one month after denervation, whereas a sharp reduction of AchE afterwards. AchE could not be stained after five month denervation.
Objective To establish an animal model for repairing the sciatic nerve defect with a biodegradable poly D,L-lactic acid/nerve growth factor (PDLLA/NGF) that can control the release conduit in rats and to observe an effect of the conduit on the sciatic nerve regeneration. Methods The PDLLA conduit and the PDLLA/NGF-controlled release conduit (NGF 450 U per conduit) were madewith the solvent-volatilixation method. Forty male SD rats were randomly and equally divided into 4 groups. The middle segments (10 mm) of the sciatic nerves of the rats were excised and were then repaired with the sciatic nerve autograft(Group A), with the PDLLA conduit (Group B), with the PDLLA conduit and an injection of NGF (30 U) into the conduit (Group C), and with the PDLLA/NGF controlled-release conduit (Group D), respectively, with the 10-mm nerve defect left behind. Three months after operation, the morphologic parameters of the nerve regeneration were observed and evaluated under light microscope and electron microscope, and the image analysis was also made. Results Three months after operation, porous adherence between the conduit and the surrounding tissues could be observed. The conduit presented a partial biodegradation but still remainedintact in the outline and the proximal nerve regenerated through the conduit cavity. Based on the histological observation, the quantity, uniformity, and maturity of the nerve fiber regeneration in Groups A and D were better than those in Groups B and C. The image analysis indicated that there were no significant differences in the nerve fiber diameter, axon diameter or myelin thickness between Group A and Group D (P＞0.05). However, all the parameters in Groups A and D were better than those in Groups B and C (P＜0.05). Conclusion The PDLLA/NGF-controlled release conduit can effectively promote the sciatic nerve regeneration of rats. Its morphological index is similar to that of the nerve autograft.
In this experiment ,the sciatic nerves or twen-ty-eight rats were cut and then anastomosed withbiological adhesive agent or by suture in randonand the latter as control. The biological adhesive a-gent from human plasma was composed of fibrino-gen coagulase and medullary sheath of the nervetaken at the anasomosis region were studied histol-gically. The results of the experimental group wsasignificantly superior to the control.
OBJECTIVE: To study the expression of interleukin-1 receptor in normal mice sciatic nerves and in transected sciatic nerves treated with or without extrinsic interleukin-1 locally at different periods. METHODS: Seventy-two KM mice were equally divided into two groups. All the left sciatic nerves were transected. The stumps in experimental group were soaked in liquid with interleukin-1, whereas those in control group without interleukin-1. Then all the stumps were repaired end to end. At the 3rd hour, 1st day, 3rd day, 7th day, 14th day, and 28th day after operation respectively, every proximal stump was dissected and the expression of interleukin-1 receptor was carried out by immunohistochemistry method (LSAB method). The expression level of interleukin-1 of ten normal sciatic nerves of mice was studied, too. RESULTS: Normal nerves showed interleukin-1 receptor expression on the membrane of Schwann cells. After nerve injury, the interleukin-1 receptor expression increased biphasically in both groups, but the intensity of increase was lower in the experimental group than in the control group. CONCLUSION: Schwann cell is the target cell of interleukin-1.