In the cervix, many biochemical and biophysical changes have been reported to occur at term. The nonpregnant cervix is a firm, rigid structure compared to the edematous compliant cervix at delivery. Cervical ripening involves an elemental change in the arrangement and concentration of the collagen fibers, resulting in a dramatic reduction in the tensile strength of the tissue (40). Collagen bundles tightly surrounded by proteoglycans are broken up at delivery. This observation is confirmed by cervical compositional studies that report a decrease in collagen concentration by 70% at term (41). Prostaglandins and PG inhibitors may be involved in the rate of synthesis and secretion of collagenase or procollagenase, the concentration of collagenase inhibitors (anticol lagenase and 2-macroglobin), and the concentration and activity of collagenase activators (42). Within 6 h of systemic or local PGE2 administration, biochemical changes are reported to occur in the unripened cervix, similar to those seen in spontaneously ripened cervix, without a measurable concomitant increase in myometrial activity (42). In vitro studies on cervical smooth muscle demonstrated a relaxation effect by PGE2, whereas PGF2α produced either no change or increased activity (43,44). Delineation of the separate roles of PGE2 and PGF2α on cervical ripening or uterine contractions has proven to be difficult, but it is clear that they are both involved in the control of parturition. Several different studies have suggested that PGE2 predominates in early labor, implicating a strong role in cervical ripening, whereas PGF2α may dominate during late labor, possibly playing a role in stimulating or maintaining uterine contractions (45,46). Leukotrienes C4 and D4 have been associated with uterine contractions even in the presence of suppressed levels of PGF2α during term and preterm labor (47). Certain PG, such as oxytocin, have been implicated in the intracellular release of calcium in the myometrium that may stimulate contraction. This action could lead to an increase in intracellular cAMP, eventually producing sequestration of calcium in the mitochondria and sarcoplasmic reticulum, and result in relaxation of the myometrial cell (48,49). Additionally, PG have been implicated in inducing formation of gap junctions between myometrial cells. Gap junction formation is critical for the efficient and rapid spread of action potentials from cell to cell and the synchronized generation of contractions in the entire myometrium. The suppression of these events has provided the rationale for the use of nonsteroidal antiinflammatory drugs (NSAID) as tocolytic agents.