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  • Title: Effects of prostaglandins on oviductal motility and egg transport.
    Author: Spilman CH, Harper MJ.
    Journal: Gynecol Invest; 1975; 6(3-4):186-205. PubMed ID: 809315.
    Abstract:
    The effects of prostaglandins (PGs) on muscular activity of the oviductal isthmus and on the rate of tubal egg transport are reviewed. In consideration of the available data a mechanism by which PGs contribute to the physiological control of egg transport is suggested. In vivo experiments have demonstrated that E-series PGs relax while F-series PGs stimulate muscular activity of the oviduct in humans, subhuman primates and rabbits. These effects are mutually antagonistic. The response of oviductal muscle to PGs appears to be affected by ovarian steroids; progesterone increases the response to PGE1 and decrease the response to PGF2alpha. Oviductal tissue concentrations of PGF increase in a distal to proximal sequence following ovulation-induction in the rabbit. Also, proximal isthmus binding of PGE1 t tended to be greater in 72-hour pregnant rabbits than in estrous rabbits, while binding of PGF2alpha was greater in estrous than in 72-hour pregnant animals. It is suggested that the preovulatory increase in ovarian estradiol secretion stimulates PGF synthesis in the oviductal tissue in a sequential fashion, the peak value occurring when the oviductal isthmus is most sensitive to stimulation by PGF2alpha. The changes in tissue concentration of PGF and in sensitivity to PGF2alpha could contribute to occlusion of the isthmus and prevent premature passage of eggs into the uterus. An increase in ovarian progesterone secretion after ovulation may decrease tissue PGF, decrease the response to PGF2alpha stimulation, and increase the response to PGF1. These changes may then allow a progressive movement of eggs through the isthmus into the uterus. Several questions regarding this proposed mechanism remain unanswered. The effects of (PGs) prostaglandins on muscular activity of the oviductal isthmus and on the rate of tubal egg transport are reviewed. In consideration of the available data, a mechanism by which PGs contribute to the physiological control of egg transport is suggested. In vivo experiments have demonstrated that PGEs relax while PGFs stimulate muscular activity of the oviduct in humans, subhuman primates and rabbits. These effects are mutually antagonistic. The response of oviductal muscle to PGs appears to be affected by ovarian steroids; progesterone increases the response to PGE1 and decreases the response to PGF2alpha. Oviductal tissue concentration of PGF increase in a distal to proximal sequence following ovulation-induction in the rabbit. Also, proximal isthmus binding of PGE1 tended to be greater in 72-hour pregnant rabbits than in estrous rabbits, while binding of PGF2alpha was greater in estrous than in 72-hour pregnant animals. It is suggested that the preovulatory increase in ovarian estradiol secretion stimulates PGF synthesis in the oviductal tissue in a sequential fashion, the peak value occurring when the oviductal isthmus is most sensitive to stimulation by PGF2alpha. The changes in tissue concentration of PGF and in sensitivity to PGF2alpha could contribute to occlusion of the isthmus and prevent premature passage of eggs into the uterus. An increase in ovarian progesterone secretion after ovulation may decrease tissue PGF, decrease the response to PGF2alpha stimulation, and increase the response to PGE1. The changes may then allow a progressive movement of eggs through the isthmus into the uterus. Several questions regarding this proposed mechanism remain unanswered.
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