REOXYGENATION OF ANOXIC PERIPHERAL-NERVE MYELINATED AXONS PROMOTES REESTABLISHMENT 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 an d Ca; i.e., an initial influx of Na and loss of K is coupled to subseq uent Ca accumulation [7]. In the present study, we examined the abilit y of PNS axons to recover normal elemental composition following oxyge n deprivation. Thus, electron probe X-ray microanalysis was used to de termine the effects of post-anoxia reoxygenation on the concentrations of elements (i.e., Na, K, Cl, Ca, Mg, P and S) in rat posterior tibia l nerve myelinated axons and Schwann cells. Results indicate that foll owing 180 min of anoxia, peripheral nerve reoxygenation (60 and 120 mi n) promoted progressive recovery of normal elemental composition in ax oplasm and mitochondria of small, medium and large diameter tibial ner ve fibers. Our observations also indicate that small axons recovered n ormal elemental concentrations more rapidly than larger counterparts. Schwann cells and myelin exhibited only modest elemental disruption du ring anoxia from which reoxygenation promoted full reparation. The abi lity of peripheral nerve axons to restore normal elemental composition during post-anoxia reoxygenation is in marked contrast to the exacerb ation of elemental deregulation which ensued during in vitro reoxygena tion of anoxic rat CNS fibers [14]. This differential response to reox ygenation represents a fundamental difference in the pathophysiology o f myelinated axons in the CNS and PNS.