RT Journal Article SR Electronic T1 Platelet-activating factor reduces spinal cord blood flow and causes behavioral deficits after intrathecal administration in rats through a specific receptor mechanism. JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 1064 OP 1070 VO 261 IS 3 A1 A I Faden A1 P Halt YR 1992 UL http://jpet.aspetjournals.org/content/261/3/1064.abstract AB 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.