Two waves of prenatal mortality reaching 30-45% in total occur during early and middle gestation in commercial swine. Mechanisms for this loss are not known but poor blood supply to the developing fetus is postulated to be a leading cause. Lymphocytes are transiently recruited to implantation sites in porcine pregnancy, and they may regulate endometrial angiogenesis. My study documents dynamic changes in gene expression in porcine endometrium, lymphocytes, endothelium and trophoblast associated with healthy and arresting sites during early and mid pregnancy. Maternal lymphocytes and endothelial cells expressed more angiogenic transcripts than trophoblast in healthy sites. At arresting sites, lymphocytes and endothelial cells expressed fewer angiogenic transcripts. Similar differences were observed at the protein level. Proinflammatory cytokine transcription was elevated at arresting sites. Histological analyses revealed irregular endothelium, fragmented elastin and excessive collagen in the endometrial arteries associated with arresting fetuses. These data indicate that fetal loss is a process precipitated by endometrial vascular failure.