Reoxygenation of anoxic peripheral nerve myelinated axons promotes re-establishment of normal elemental composition

Previously we have shown that in vitro anoxia of rat peripheral nerve myelinated axons causes sequential deregulation of axoplasmic Na, K and Ca; i.e., an initial influx of Na and loss of K is coupled to subsequent Ca accumulation [7]. In the present study, we examined the ability of PNS axons to recover normal elemental composition following oxygen deprivation. Thus, electron probe X-ray microanalysis was used to determine the effects of post-anoxia reoxygenation on the concentrations of elements (i.e., Na, K, Cl, Ca, Mg, P and S) in rat posterior tibial nerve myelinated axons and Schwann cells. Results indicate that following 180 min of anoxia, peripheral nerve reoxygenation (60 and 120 min) promoted progressive recovery of normal elemental composition in axoplasm and mitochondria of small, medium and large diameter tibial nerve fibers. Our observations also indicate that small axons recovered normal elemental concentrations more rapidly than larger counterparts. Schwann cells and myelin exhibited only modest elemental disruption during anoxia from which reoxygenation promoted full reparation. The ability of peripheral nerve axons to restore normal elemental composition during post-anoxia reoxygenation is in marked contrast to the exacerbation of elemental deregulation which ensued during in vitro reoxygenation of anoxic rat CNS fibers [14]. This differential response to reoxygenation represents a fundamental difference in the pathophysiology of myelinated axons in the CNS and PNS.