Recent experimental evidence has implicated the potent phospholipid inflammatory mediator, platelet activating factor (PAF) in the pathogenesis of necrotizing enterocolitis (NEC). We have developed a neonatal rat model of NEC using two risk factors for human NEC, asphyxia (A) and formula feedings (F). In this model, the clinical signs and intestinal lesions are similar to those of human NEC. The biological effects of PAF is mediated through the PAF Receptor (PAF-R), the gene of which has recently been isolated and sequenced. This experiment measured PAF-R gene expression in the intestine of newborn rats subjected to (A) and (F). Intestinal samples were studied from 2 control groups of starved (S), non-asphyxiated (NoA) pups, which differed only by method of birth; c-section vs natural birth. The two experimental groups differed from the c-section control group only in exposure to (A) or (F). Intestine samples from the 4 pups in each group were harvested and intestinal PAF-R mRNA was quantified by competitive RT-PCR using a 585 bp competitor RNA of rat PAF-R (gift of H. Wang and Dr. W. Hsueh). Following the competitive RT-PCR amplification, reaction products were separated by electrophoresis and transcript and competitor cDNA bands were quantified by phosphorimaging. Mean PAF-R transcript levels (molecules × 106 PAF-R mRNA per ug total RNA) were similar between control groups (4.01 ±1.91 vs 7.37±1.05) but increased significantly in the experimental pups subjected to (A) (13.9±1.92) and (F) (15.1 ±5.09). These data suggest that in the newborn rat model of NEC the stresses of (A) and (F) increase PAF-R gene expression. The increased PAF-R gene activity in newborn rats following exposure to risk factors for human NEC further supports the role of PAF in the pathogenesis of NEC.