Altered norepinephrine metabolism following experimental spinal cord injury: Part 1: Relationship to hemorrhagic necrosis and post-wounding neurological deficits

Abstract

✓ Experimentally injured spinal cord tissues were chemically examined for changes in norepinephrine (NE), serotonin, and dopamine; remarkable NE metabolic alterations were found. The amine doubled in 30 minutes, quadrupled in 1 hour, and thereafter slowly declined to approach control values at 4 hours. Comparisons between injured tissue NE content and the presence of central gray hemorrhages and necrosis were consistently found, and profound increases in NE were universally associated with massive central hemorrhages. Within 2 hours of injection of minute quantities of pure NE into the spinal gray matter, large central hemorrhages appeared that closely resembled the lesions associated with severe spinal cord injury. We have hypothesized that toxic quantities of tissue NE induce intense vasospasm which impedes or arrests cord perfusion and causes the neuronal necrosis, vascular rupture, and parenchymal self-destruction manifest as central hemorrhagic necrosis. Thus, excess NE liberated within traumatized tissue may act to depress or halt electrical activity of adjacent fibers and neurons, producing the neuronal response of transient weakness or paralysis. Permanent loss of function ensues as the electrically depressed spinal cord tissue also undergoes hemorrhagic autodestruction.