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  • Title: [Fetal causes of the onset of labour. A kybernetic model (author's transl)].
    Author: Warkentin B.
    Journal: Arch Gynakol; 1977 Jan 27; 222(1):15-27. PubMed ID: 576384.
    Abstract:
    The question of initiation of labour is not yet solved. A fetal fixing of the date would be ingenious. On the one hand the fet is endangered by prematurity, on the other hand by placental insufficiency in postmaturity. Fetuses with comparatively lighter placenta remain in average shorter in utero until spontaneous initiation of labour than those with comparatively heavier placenta. This fact leads to the assumption of a relative placental insufficiency as a determining factor of the onset of labour. A further inquiry demonstrates, that babies born after premature termination of pregnancy about the term - either by induction of labour or by primary sectio caesarea - are heavier and longer than those born after spontaneous labour. This leads to the assumption of a prenatal weight loss of the infant before spontaneous initiation of labour. This weight loss is caused by diminution of water content and relative placental insufficiency. This relative placental insufficiency also leads to a diminution of amniotic fluid, which is swallowed by the "hungry" fet in a greater amount. Altogether a diminution of uterine volume is resulting, which is accomplished by a diminution of uterine wall tension. The coordination of uterine activity, which precedes delivery, is combined with the ripening of the cervix. The ripening of the cervix also leads to a retraction of myometrium and thus to a further diminution of uterine wall tension. It is concluded, that a diminution of uterine volume, causes by fetal weight loss and diminution of amniotic fluid, leads to a reduction of uterine wall tension, which is supported by the ripening of the cervix. This reduction of uterine wall tension is the precondition of the increasing coordination of activity, which precedes delivery. The causal factor in the onset of labor has not yet been clearly identified, but fetal determination of the birth term is 1 reasonable explanation. Survival of the fetus is endangered by premature birth on the 1 hand, and by postmaturity placental insufficiency on the other. Studies have shown that the fetus with a larger placenta remains longer in the uterus, and this suggests that placental insufficiency (smaller placenta = less diffusion) may determine the onset of labor. Further investigations have revealed that premature births (e.g., induction of labor, primary Caesarean section) produce heavier and longer infants than do spontaneous births. This surprising observation suggests that the fetus suffers weight loss, due to dehydration. Relative placental insufficiency leads to a reduction in amniotic fluid, as the growing, ''hungry'' fetus takes in more and more water. The result is diminished uterine volume and slackening of the myometrium. Coordination of uterine activity with cervical maturation causes a retraction of the myometrium and further relaxation of the uterine musculature. This is the precondition and signal for labor and birth.
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