Hyperbaric oxygenation is known to affect energy metabolism and endothelial cell structure and function, but its effects on peripheral nerve have not been reported. We investigated whether it would (i) reverse established streptozotocin-induced diabetic neuropathy, a condition in which endoneurial hypoxia exists; (ii) affect energy metabolism in nerve; and (iii) alter the blood-nerve barrier. Sprague-Dawley rats that had been diabetic for 3 months and age-matched controls were used in these studies. One diabetic group and one control group were treated with hyperbaric oxygenation (2 atm for 2 h, 5 days/week) for 4 weeks. Identical groups remained in room air. Sciatic nerve adenosine triphosphate (ATP), creatine phosphate, lactate, and glucose concentrations showed similar changes at rest in both room air and after hyperbaric oxygenation. Nerves of control and diabetic groups exhibited increased lactate production and increased utilization of glucose, ATP, and creatine phosphate after 15 min of anoxia. The albumin blood-nerve barrier index was increased in control and diabetic nerves after hyperbaric treatment. Nerve conduction velocity was reduced in the diabetic-room air group and not improved by hyperbaric oxygenation. Caudal nerve action potential, which was significantly reduced in this group, was normalized after hyperbaric treatment. Resistance to ischemic conduction failure was increased in untreated diabetic nerve but not significantly different from controls after hyperbaric exposure. These findings indicate that treatment with hyperbaric oxygenation will partially reverse the neuropathy encountered in chronic diabetes. The biochemical changes are suggestive of enhanced nerve energy metabolism induced by hyperbaric oxygenation. The altered albumin blood-nerve barrier index presumably results from the action of free radicals on endothelial cells.
Low, Schmelzer, Ward, Curran, Poduslo, , , , (1988). Effect of hyperbaric oxygenation on normal and chronic streptozotocin diabetic peripheral nerves. Experimental neurology, 1988 Jan;99(1):201-12. https://www.ncbi.nlm.nih.gov/pubmed/3335240