Oviduct function in pigs, with particular reference to the pathological condition of polyspermy

Abstract

Because the exceptionally high incidence of polyspermic fertilisation has been emphasised as a major defect in systems of in vitro fertilisation in pigs, the aetiology of the condition has been analysed in a series of experiments in vivo in the search for a common underlying cause and possible means of mitigation. Whereas the defense mechanism against polyspermy in pig oocytes is classically viewed as a zona reaction, more recent evidence suggests a secondary block at the vitelline surface. Both blocks may be compromised in situations leading to polyspermy, although deleterious influences seem to be expressed principally in an inadequate zona block, as judged by the presence of perivitelline spermatozoa. Postovulatory aging of mammalian oocytes prior to sperm penetration leads to polyspermy, as can be demonstrated in pig eggs. The primary lesion may concern the cortical reaction, owing to a delayed and incomplete exocytosis of the vesicular contents. Eggs ovulated after gonadotrophin treatment during the luteal phase of the cycle show a high incidence of polyspermic penetration (60.6%), as do those shed at estrus in animals treated with progesterone systemically (40%) or by local microinjections in the oviduct wall (32.3%). Whereas progesterone may be modifying interactions of the gametes and responses of the egg organelles in all four above experimental situations, enhanced numbers of spermatozoa ascending a more patent isthmus appear to be the principal cause of polyspermy. Support for this hypothesis comes from isthmus resection with re‐anastomosis of remaining portions of the oviduct (32.4% polyspermy), and surgical insemination directly into the oviducts (33.8% polyspermy). Recent experiments draw attention to a role for oviduct epithelial glycoproteins in modulating the extent of polyspermy in vitro. The role of such oviduct macromolecules in gamete interactions in vivo is considered. Copyright © 1991 Wiley‐Liss, Inc.