Differential Effects of Hypoosmotic Hyponatric Swelling on A and C Fibers

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Abstract
The differential effects of exposure to a moderately hypoosmotic hyponatric solution (0.35 isoosmotic, Na+ 36 mmol/l) on conduction in myelinated (A) and unmyelinated (C) axons were studied in vitro on compound action potentials of rabbit vagus nerves in which the perineurial sheath was undisturbed. Controls were incubated at 37.degree. C in isoosmotic isonatric solution for 5 h (group 1a, n = 7) or 7 h (group 3, n = 3). Other controls were incubated in isoosmotic isonatric solution for 2 h followed by 3 h in isoosmotic hyponatric (Na+ 36 mmol/l) solution (group 1b, n = 6); experimental nerves were incubated in isoosomtic isonatric solution for 2 h followed by 3 h hypoosmotic hyponatric solution (group 2, n = 7) and, to study recovery, a further 2 h in isoosmotic isonatric solution (group 4, n = 8). In group 1b, isoosmotic hyponatric exposure approximately doubled the latency of the A-component (A-CAP) and decreased the A-CAP amplitude to 44 .+-. 8% of control; the amplitude of the C-component decreased to 64 .+-. 15% of control. Hypoosmotic hyponatric exposure increased the latency of the A-CAP by 82 .+-. 10% (mean .+-. SE, P < 0.001) and extinguished A-CAP within 20 min while the latency increase of the C-component (C-CAP) was more than twice as great and extinction slower and often incomplete; neural wet weight increased 34 .+-. 4% and neural Na and K contents decreased 55 and 42%, respectively. Recovery in isoosmotic isonatic solution (group 4) was absent or very small in the case of A-CAP as regards latency and amplitude but was complete for C-CAP amplitude. Neural wet weights and Na content also recovered fully, but neural K content recovered only .apprx. 45%. EM revealed hypoosmotic hyponatric structural damage to the larger myelin sheaths; the axons themselves were unaffected. It is probably inadvisable to attempt selective conduction block of sensory C-fibers by application of hypoosmotic solutions to peripheral nerves.