The fetus becomes stressed because it approaches the inherent space limitations of the uterus, resulting in the fetus’s anterior pituitary gland to release ACTH (Adrenal corticotropic hormone). Fetal cortisol promotes the synthesis of three enzymes (17alpha Hydroxylase, 17-20 Desmolase, and Aromatase) to convert progesterone to estradiol. Estradiol encourages myometrial (or uterine) contractions become more active and contractions are more noticeable. Secretory activity also increases in the vagina and cervix, with the production of mucus providing lubrication for the easier passage of the fetus. Mucus secretion also helps wash out the cervical seal of pregnancy. Fetal corticoids also cause the placenta to synthesize PGF2alpha to help eliminate the progesterone block. Corpus luteum starts to regress, facilitating the decline in progesterone. Relaxin, a glycoprotein, is produced by PGF2alpha and stimulates the softening of the connective tissue in the cervix and promotes elasticity of the pelvic ligaments, allowing easier passage of the fetus. Calf fetus rotates so that the front feet and head are positioned towards the rear (posterior) of the dam. Contracting uterus begins to push the fetus towards the cervix, applying pressure to the cervix. Pressure on the cervix activates pressure-sensitive neurons located in the cervix that synapse in the spinal cord and eventually synapse with oxytocin producing neurons in the hypothalamus. Oxytocin acts to facilitate myometrial contractility initiated by estradiol and PGF2alpha. As pressure on the cervix increases, oxytocin secretion increases; force of contraction of the myometrial smooth muscle begins to peak. Fetus enters cervical canal; first stage complete.
Strong myometrial and abdominal contractions continue until the calf is expelled from the birth canal. The feet and head of the fetus put pressure on the fetal membranes until they rupture, resulting in a substantial loss of amniotic and allantoic fluid. Fetus becomes hypoxic (or deprived of adequate oxygen levels), and this hypoxia promotes fetal movement which in turn promotes further uterine contractions.
The car-uncles (or chronic villi) becomes dislodged from the uterine wall This release is believed to be brought about by powerful vasoconstriction of arteries in the villi. Further myometrial contractions, as well as the beginning of the involution of the uterus, help expel the fetal membranes.
The teats of the cow will start to fill up, looking full and distended, with the teat plugs often starting to come out. Most cows will show these signs 24 hours prior to calving.
This “gunk” is the afterbirth, the remains of the placenta and fetal membranes.
