sodium-bicarbonate and Diabetic-Neuropathies

We explore whether the prevalence of sensory deficits in diabetic neuropathy can be explained by diffuse endoneurial hypoxia. Isolated ventral and dorsal rat spinal roots incubated in 2.5 or 25 mM extracellular glucose were transiently exposed to hypoxia (30 min) in a solution of low buffering power. Compound nerve action potentials and extracellular direct current potentials were continuously recorded before, during, and after hypoxia. In both ventral and dorsal roots incubated in 2.5 mM glucose, sensitivity to hypoxia and posthypoxic recovery were similar. In contrast, hypoxia in 25 mM glucose preferentially induced electrophysiological damage in dorsal roots as indicated by a lack of posthypoxic recovery. This observation was not made in the presence of 25 mM bicarbonate, which suggests involvement of nerve acidosis. In conclusion, the different sensitivity of sensory and motor fibers to hyperglycemic hypoxia supports the hypothesis that hypoxia has an important role in the pathogenesis of diabetic neuropathy.

Topics: Action Potentials; Animals; Bicarbonates; Cell Hypoxia; Diabetic Neuropathies; Glucose; Motor Neurons; Neurons, Afferent; Organ Culture Techniques; Osmolar Concentration; Peroneal Nerve; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Spinal Nerve Roots