Platelet-activating factor reduces spinal cord blood flow and causes behavioral deficits after intrathecal administration in rats through a specific receptor mechanism.

Platelet-activating factor (PAF) is a phospholipid that has been implicated in the pathophysiology of delayed tissue damage after various forms of brain injury including ischemia, hypoxia and trauma. To examine its effects in the spinal cord, PAF was administered intrathecally to rats. PAF caused dose-dependent (30-100 nmol) decreases in spinal cord blood flow, in motor function or in survival. These actions were not reproduced by the biologically inactive precursor lyso-PAF or the enantiomer of this alkyl-phospholipid, which is not active at PAF receptors. PAF-induced changes were blocked completely by the selective receptor antagonist WEB 2170. Together, these findings demonstrate that PAF can alter spinal cord blood flow and motor function through a specific receptor mechanism, suggesting that this phospholipid may play a role in secondary tissue damage after spinal cord injury.