Abstract
Axoplasmic transport of cat sciatic nerves was studied in vitro in a chamber in which maximal α action potentials could also be elicited. After initiation of N2 anoxia, electrical responses fell to zero at an average time of 22 min. A shorter time to zero of 11 min was seen during a second period of anoxia. A good recovery of both action potential responses and axoplasmic transport occurs after a period of anoxia lasting 1–1.5 hr. An apparent failure of recovery of axoplasmic transport was seen after 2 hr of anoxia with a good recovery of electrical responses. Axoplasmic transport tended to return toward normal when more time was allowed for recovery after anoxia. An adequate supply of ∼P was shown to be present by measurement of ATP and creatine phosphate levels. The delay in recovery of transport thus signifies a failure of utilization of ∼P by the transport mechanism. Longer periods of anoxia and recovery were limited in vitro and for this reason, ischemic anoxia was produced in vivo. Blood pressure cuffs were placed on the upper thigh of cats and maintained for times of 1–8 hr at pressures of 300–310 mm Hg. Then, recovery times up to 7 days were allowed. It was shown that axoplasmic transport could gradually recovery after an anoxia lasting up to 6–7 hr if sufficient recovery times were allowed. A possible explanation for the delay in the recovery of axoplasmic transport and the disassociation in the earlier recovery of electrical responses as against the recovery of transport was discussed.