Abstract
Successful nerve regeneration depends on the type of injury, the method of repair and the metabolic status of the animal. A state similar to poorly controlled Type I diabetes mellitus in man was induced and maintained in rats using streptozotocin. This provided a model for the study of nerve regeneration in diabetes over a period of 150 days. Two methods of nerve injury (crush and transection) and three methods of repair (epineurial suture, nerve autograft and freeze-thawed skeletal muscle autograft) were compared using electrophysiological and histological methods. The diabetic state did not affect the degree of recovery of nerve conduction velocity after nerve injury. By 150 days, recovery to control values of axon and nerve fibre diameters was not attained. Recovery of axon and fibre diameter was significantly poorer in the diabetic nerve crush group compared with the non-diabetic nerve crush group. It is concluded that this was because of poorer regeneration in diabetic nerve.
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