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  • Title: The role of prostaglandins in human parturition.
    Author: Gibb W.
    Journal: Ann Med; 1998 Jun; 30(3):235-41. PubMed ID: 9677008.
    Abstract:
    Parturition is the process of giving birth, and the molecular mechanisms involved are still to be elucidated. Among the various factors involved prostaglandins appear to have an important role. They are synthesized within the human fetal membranes (amnion and chorion) and decidua and act to ripen the cervix, change membrane structure and contract the myometrium. Prostaglandin concentrations increase in amniotic fluid prior to myometrial contractions, and the activity of prostaglandin H synthase (PGHS) increases in the chorion laeve and amnion at labour. This increase is due to increased expression of the PGHS-2 isoenzyme rather than the PGHS-1 isoenzyme. In animal pregnancy, there is also an increase in the expression of the PGHS-2 isoenzyme, and in both human and animal pregnancies this increase appears to occur in the fetal tissues rather than in the maternal tissues. Prostaglandin metabolism also plays an important role in altering prostaglandin output by the human fetal membranes. Prostaglandin dehydrogenase (PGDH) activity decreases in certain cases of preterm labour, and at term it decreases in the area of the chorion laeve covering the cervix. This may allow active prostaglandins produced by the amnion and chorion to access the cervix and myometrium. Recent studies have indicated that glucocorticoids may be important in regulating prostaglandin formation within the human fetal membranes by increasing expression of PGHS-2 in the amnion and decreasing PGDH activity in the chorion. Prostaglandin formation is also important in infection-induced preterm labour and both phospholipase and PGHS-2 activities can be increased by various cytokines. Prostaglandins are important for the onset of both term and preterm parturition and their effects may result from changes in prostaglandin synthesis, prostaglandin metabolism and expression of various prostaglandin receptors.
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