Author(s): Hawk HW
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Abstract Fertilization failure, mostly due to absence of sperm in the oviducts, is a major cause of reproductive inefficiency of farm animals. Sperm may be transported to the oviducts of cattle and sheep within a few minutes after mating or insemination, but these sperm probably fertilize few ova. Slower transport, with establishment of sperm populations in each segment of the reproductive tract, requires a few to several hours. In swine, sperm capable of fertilizing ova reach the oviducts in less than 1 h. Smooth muscle contractions of the reproductive tract, ciliary beats, fluid currents, and flagellar activity of sperm are primary mechanisms of sperm transport. Sperm become hyperactive in the oviducts in association with capacitation. Most sperm in an inseminate drain from the female reproductive tract within a few minutes or hours after insemination; remaining sperm are removed from the tract by slower drainage or phagocytosis. Sperm survival and transport in estrous ewes is reduced drastically by pastures with high estrogen content and by regulating estrus with progestogen or prostaglandin F2 alpha. The cervix is the initial site of inhibition of sperm transport in ewes, and endocrine imbalances probably are the basis of inhibition. Sperm transport problems generally are associated with immobilization and death of sperm in the uterus and anterior segments of the cervix within 2 h after mating. After gilts are inseminated with frozen-thawed semen, relatively few sperm are retained in the reproductive tract, apparently accounting for lowered fertilization rates. Sperm transport has been improved by adding to semen or administering to females such compounds as prostaglandin F2 alpha, oxytocin, estradiol, phenylephrine, or ergonovine. Estradiol, prostaglandin F2 alpha, phenylephrine, and ergonovine administered to rabbits at insemination each increased fertilization rates.
This article was published in J Dairy Sci
and referenced in Journal of Metabolic Syndrome