Abstract

The objective of this article is to review the role of uterine defense mechanisms in natural resistance to chronic or persistent endometritis. A breakdown of uterine physical clearance mechanisms is currently believed to play a major role in susceptibility to persistent endometritis. Mares with increased susceptibility to persistent endometritis have impaired myometrial contractility in response to an acute inflammation, resulting in an accumulation of fluid and inflammatory products within the uterine lumen. The origin of this defect remains unknown. Recent studies have demonstrated that spermatozoa trigger PMN chemotaxis into the uterine lumen. This observation suggests that a transient endometritis is a normal physiological response to breeding. However, in mares with impaired uterine defense mechanisms, the condition may develop into a persistent endometritis and subsequent subfertility. In contrast to spermatozoa, seminal plasma has a suppressive effect on complement activation and PMN chemotaxis (65). The exact role of seminal components in breeding-induced inflammation needs further investigation. Based on current information, persistent endometritis can be divided into (1) sexually transmitted diseases (STD), (2) chronic infectious endometritis, (3) persistent breeding-induced endometritis, or (4) chronic degenerative endometritis (endometrosis). While treatments of STD and chronic infectious endometritis need to be directed against a specific microbial agent, treatment of mares with persistent breeding-induced endometritis should assist the uterus to physically clear contaminants and inflammatory products. This can be achieved by the use of uterine lavage with sterile saline, or by the administration of uterotonic drugs, such as oxytocin or PGF 2α.

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