Susceptibility of isolated rat facial nerve to anaerobic stress.

Ischemic lesions are presumed to be part of many facial nerve pathologies, such as Bell's palsy. The response of facial nerve to hypoxia has not been evaluated previously in an in vitro model. In the present study, the effects of transient anaerobic stress on functional parameters and their recovery were assessed. Extratemporal rat facial nerves were desheathed and incubated in an experimental chamber using solutions containing either low (5 mM) or high (25 mM) D-glucose. In some of the experiments, 40 microM phenytoin or lidocaine was added to observe the effects of membrane stabilizing drugs. Peak height of compound nerve action potential (CNAP), extracellular direct current (DC) potential and latency were measured simultaneously during and after a 40-min period of hypoxia, induced by bubbling the solutions with N2 or application of 3 mM cyanide. This resulted in a rapid decrease of CNAP and a depolarization of the DC potential with a fast and complete post hypoxic recovery. Elevated glucose concentrations led to a slower decline in CNAP and a smaller rise of membrane potential depolarization. This was accompanied by a slower change of latency. However, post-anaerobic recovery was always diminished in the high glucose solutions. In experiments with phenytoin or lidocaine longer impulse conduction during hypoxia was observed. These findings indicate that the availability of energy-rich components underlies the complex array of physiological derangements seen in ischemia. Membrane-stabilizing drugs show an effect on signal conduction during hypoxia and need further exploration.