Mares with delayed uterine clearance have an intrinsic defect in myometrial function

Persistent, postmating endometritis affects approximately 15% of mares and results in reduced fertility and sizable economic losses to the horse-breed ing industry. Mares that are susceptible to postmating endometritis have de layed uterine clearance associated with reduced uterine contractility. Unfo rtunately, the mechanism for reduced uterine contractility remains an enigm a. The present study examined the hypothesis that mares with delayed uterin e clearance have an intrinsic contractile defect of the myometrium. Myometr ial contractility was evaluated in vitro by measuring isometric tension gen erated by longitudinal and circular uterine muscle strips in response to KC l, oxytocin, and prostaglandin F-2 alpha (PGF(2 alpha)) for young nulliparo us mares, older reproductively normal mares, and older mares with delayed u terine clearance. In addition, intracellular Ca2+ regulation was evaluated using laser cytometry to measure oxytocin-stimulated intracellular Ca2+ tra nsients of myometrial cells loaded with a Ca2+-sensitive fluorescent dye, f luo-4. For all contractile agonists, myometrium from mares with delayed ute rine clearance failed to generate as much tension as myometrium from older normal mares. Oxytocin-stimulated intracellular Ca2+ transients were simila r for myometrial cells from mares with delayed uterine clearance and from o lder normal mares, suggesting that the contractile defect did not result fr om altered regulation of intracellular Ca2+ concentration. Furthermore, no apparent age-dependent decline was observed in myometrial contractility; KC l-depolarized and oxytocin-stimulated longitudinal myometrium from young no rmal mares and older normal mares generated similar responses. However, cir cular myometrium from young normal mares failed to generate as much tension as myometrium from older normal mares when stimulated with oxytocin or PGF (2 alpha), suggesting possible age-related alterations in receptor-second m essenger signaling mechanisms downstream of intracellular Ca2+ release. In summary, for mares with delayed uterine clearance, an intrinsic contractile defect of the myometrium may contribute to reduced uterine contractility f ollowing breeding.