The association of endometriosis and infertility is well know. However, the exact mechanisms involved remain unclear. To study the effect of endometriosis on fertility, an experimental model was developed using New Zealand White rabbits. Endometrium obtained from one uterine horn was surgically implanted into the peritoneum, and the viability of the implants was demonstrated histologically. Adipose tissue was implanted in another group of animals which served as a control. The induction of endometriosis significantly impaired fertility rates (25%) as compared with the control group (75%). The decrease in fertility was independent of adhesion formation and primarily due to a defect in ovulation; however, a postovulatory effect cannot be excluded. Peritoneal fluid prostaglandin (PG) F concentrations increased significantly after the induction of endometriosis, whereas PGE concentrations and the PGF:PGE ratio showed no change. There was no change in PGF or PGE levels in the control group. The increased PGF in peritoneal fluid may alter follicular rupture, ovum transport, corpus luteum function, or implantation, thus representing a mechanism by which endometriosis may cause infertility.