Okay, attack plan delta
Okay. So walking and patience and a sweep and all that have done nothing so far. I am now trying to encourage labour by reading (occasionally out loud, because the fetus is not passive in this process!) the uptodate articles on the mechanism and management of labour.
Get this: "Labor is a physiological event involving a sequential, integrated set of changes within the myometrium, decidua, and uterine cervix that occurs sometimes gradually over a period of days to weeks and sometimes rapidly over minutes to hours and culminates in delivery of the fetus. Biochemical connective tissue changes in the uterine cervix appear to precede uterine contractions and cervical dilation, and all of these events usually occur before rupture of the fetal membranes."
AND "Uterine contractions during active labor have two major functions: to dilate the cervix and to push the fetus through the birth canal. However, the fetus is not merely the passive recipient of these forces, rather, its ability to successfully negotiate the pelvis is dependent upon the complex interaction of three mechanical variables, known as the "three Ps": the powers, the passenger, and the passage."
Oh, and get a load of this: "Term labor may be regarded physiologically as a release from the inhibitory effects of pregnancy on the myometrium, rather than as an active process mediated by uterine stimulants. As an example, strips of myometrium obtained from a quiescent uterus at term and placed in an isotonic water bath will contract vigorously and spontaneously without added stimuli [3,4]. Nevertheless, both inhibitory and stimulatory mechanisms likely play a role in uterine activity."
That's COOL.
Now all I have to do is mentally stimulate the release from inhibitory effects. Lol.
See, like this:
PHYSIOLOGICAL PHASES OF MYOMETRIAL ACTIVITY - The regulation of uterine activity during pregnancy can be divided into four distinct physiologic phases [5,6]:
Phase 0: inhibitors active - Throughout most of pregnancy the uterus is maintained in a state of functional quiescence through the action of various putative inhibitors including, but not limited to:
Progesterone
Prostacyclin (prostaglandin I-2)
Relaxin
Parathyroid hormone-related peptide
Nitric oxide
Calcitonin gene-related peptide
Adrenomedullin
Vasoactive intestinal peptide.
Phase 1: myometrial activation - As term approaches the uterus becomes activated in response to uterotropins, such as estrogen. This phase is characterized by increased expression of a series of contraction-associated proteins (CAPs) (including myometrial receptors for prostaglandins and oxytocin), activation of specific ion channels, and an increase in connexin-43 (a key component of gap junctions). An increase in gap junction formation between adjacent myometrial cells leads to electrical synchrony within the myometrium and allows for effective coordination of contractions.
Phase 2: stimulatory phase - Following activation, the "primed" uterus can be stimulated to contract by the action of uterotonic agonists, such as the stimulatory prostaglandins E2 and F2 alpha and oxytocin.
Phase 3: involution - Involution of the uterus after delivery occurs during phase 3 and is mediated primarily by oxytocin
So this is why the sweep didn't work - my myometrium obviously hasn't effectively coordinated its gap junctions and any contractions that were stimulated couldn't propogate. This is also why walking and nipple stimulation and all the rest will help, but only once the uterus is sufficiently coordinated. Until then I'm just throwing oxytocin at a brick wall.
... which is basically saying I should be patient. Damn.
*g*
I'm not alone in this though: in many ways the fetus is the key to stimulating labour.
"Considerable evidence suggests that in most viviparous animals the fetus controls the timing of onset of labor [10-12]. During the Hippocratic period, the fetus was thought to be positioned head down at term so it could kick its legs up against the fundus of the uterus, thereby propelling itself through the birth canal. While we have moved away from this simple and mechanical view of labor, the factors responsible for the initiation and maintenance of labor at term are not well defined."
Though it appears that the human method for stimulating labour may be different than other mammals - apparently sheep have been well studied, and in that species the fetus releases cortisol that is picked up by the placental unit and stimulates the biosynthesis of estrogens from progesterone to kick-start labour. But humans lack the cortisol receptor that is so important to this process in sheep.
Likewise, in mice and goats the extraplacental tissues seem to play a more important role.
So basically we have no direct idea what gets the process going, and they talk of 'assisting' the onset of labour instead of 'initiating' it because of this difficulty of telling which factor most stimulates the cascade effect.
No matter what starts things though, estrogen is definitely important. And interesting, because it seems that my body can't convert it to its most useful form, and requires the fetus to do this instead:
"Longitudinal measurements of circulating estrogen concentrations prior to the onset of labor show an increase in all primate species [51]. Because the primate placenta is an incomplete steroidogenic organ, placental estrogen synthesis has an obligate need for C-19 steroid precursors (it cannot synthesize estrogen from progesterone) [2,7]. The fetal adrenal provides an abundant C19 estrogen precursor (dehydroepiandrostenedione) directly from its intermediate (fetal) zone. In the rhesus monkey, continuous infusion of C19 precursor (androstenedione) leads to preterm delivery [52-54]. This effect is blocked by concurrent infusion of an aromatase inhibitor [54], demonstrating that conversion to estrogen is important in promoting contractions. A similar effect has been shown using a continuous intraamniotic infusion of estrogen [48]. However, systemic infusion of estrogen failed to induce delivery [48], suggesting that the action of estrogen is likely paracrine/autocrine."
Cool, eh?
Oxytocin is also incredibly important, and interestingly concentrations do not increase so much as receptor number does:
"Circulating levels of oxytocin do not change significantly during pregnancy or prior to the onset of labor [55,56]. However, myometrial oxytocin receptor concentrations increase approximately 100 to 200-fold during pregnancy, reaching a maximum during early labor [55,56,58,59]. This rise in receptor concentration accounts for the increased sensitivity of the myometrium to circulating levels of oxytocin during the second half of pregnancy."
Also: "Studies examining fetal pituitary oxytocin production, the umbilical arteriovenous difference in plasma oxytocin concentration, amniotic fluid oxytocin levels, and fetal urinary oxytocin output demonstrate conclusively that the fetus secretes oxytocin into the maternal circulation [55,60]. Furthermore, the calculated oxytocin secretion rates from the fetus suggest an increase from a baseline of 1 mU/min prior to labor to approximately 3 mU/min after spontaneous labor."
Which is cool. They go on to say that oxytocin likely doesn't stimulate labour, but does result in more forceful uterine contractions and increases the likelihood of a successful delivery.
Okay, I'm done nerding out for now. Gonna shower and then walk the dog and
head out to New Sud to see Robyn for lunch.
Get this: "Labor is a physiological event involving a sequential, integrated set of changes within the myometrium, decidua, and uterine cervix that occurs sometimes gradually over a period of days to weeks and sometimes rapidly over minutes to hours and culminates in delivery of the fetus. Biochemical connective tissue changes in the uterine cervix appear to precede uterine contractions and cervical dilation, and all of these events usually occur before rupture of the fetal membranes."
AND "Uterine contractions during active labor have two major functions: to dilate the cervix and to push the fetus through the birth canal. However, the fetus is not merely the passive recipient of these forces, rather, its ability to successfully negotiate the pelvis is dependent upon the complex interaction of three mechanical variables, known as the "three Ps": the powers, the passenger, and the passage."
Oh, and get a load of this: "Term labor may be regarded physiologically as a release from the inhibitory effects of pregnancy on the myometrium, rather than as an active process mediated by uterine stimulants. As an example, strips of myometrium obtained from a quiescent uterus at term and placed in an isotonic water bath will contract vigorously and spontaneously without added stimuli [3,4]. Nevertheless, both inhibitory and stimulatory mechanisms likely play a role in uterine activity."
That's COOL.
Now all I have to do is mentally stimulate the release from inhibitory effects. Lol.
See, like this:
PHYSIOLOGICAL PHASES OF MYOMETRIAL ACTIVITY - The regulation of uterine activity during pregnancy can be divided into four distinct physiologic phases [5,6]:
Phase 0: inhibitors active - Throughout most of pregnancy the uterus is maintained in a state of functional quiescence through the action of various putative inhibitors including, but not limited to:
Progesterone
Prostacyclin (prostaglandin I-2)
Relaxin
Parathyroid hormone-related peptide
Nitric oxide
Calcitonin gene-related peptide
Adrenomedullin
Vasoactive intestinal peptide.
Phase 1: myometrial activation - As term approaches the uterus becomes activated in response to uterotropins, such as estrogen. This phase is characterized by increased expression of a series of contraction-associated proteins (CAPs) (including myometrial receptors for prostaglandins and oxytocin), activation of specific ion channels, and an increase in connexin-43 (a key component of gap junctions). An increase in gap junction formation between adjacent myometrial cells leads to electrical synchrony within the myometrium and allows for effective coordination of contractions.
Phase 2: stimulatory phase - Following activation, the "primed" uterus can be stimulated to contract by the action of uterotonic agonists, such as the stimulatory prostaglandins E2 and F2 alpha and oxytocin.
Phase 3: involution - Involution of the uterus after delivery occurs during phase 3 and is mediated primarily by oxytocin
So this is why the sweep didn't work - my myometrium obviously hasn't effectively coordinated its gap junctions and any contractions that were stimulated couldn't propogate. This is also why walking and nipple stimulation and all the rest will help, but only once the uterus is sufficiently coordinated. Until then I'm just throwing oxytocin at a brick wall.
... which is basically saying I should be patient. Damn.
*g*
I'm not alone in this though: in many ways the fetus is the key to stimulating labour.
"Considerable evidence suggests that in most viviparous animals the fetus controls the timing of onset of labor [10-12]. During the Hippocratic period, the fetus was thought to be positioned head down at term so it could kick its legs up against the fundus of the uterus, thereby propelling itself through the birth canal. While we have moved away from this simple and mechanical view of labor, the factors responsible for the initiation and maintenance of labor at term are not well defined."
Though it appears that the human method for stimulating labour may be different than other mammals - apparently sheep have been well studied, and in that species the fetus releases cortisol that is picked up by the placental unit and stimulates the biosynthesis of estrogens from progesterone to kick-start labour. But humans lack the cortisol receptor that is so important to this process in sheep.
Likewise, in mice and goats the extraplacental tissues seem to play a more important role.
So basically we have no direct idea what gets the process going, and they talk of 'assisting' the onset of labour instead of 'initiating' it because of this difficulty of telling which factor most stimulates the cascade effect.
No matter what starts things though, estrogen is definitely important. And interesting, because it seems that my body can't convert it to its most useful form, and requires the fetus to do this instead:
"Longitudinal measurements of circulating estrogen concentrations prior to the onset of labor show an increase in all primate species [51]. Because the primate placenta is an incomplete steroidogenic organ, placental estrogen synthesis has an obligate need for C-19 steroid precursors (it cannot synthesize estrogen from progesterone) [2,7]. The fetal adrenal provides an abundant C19 estrogen precursor (dehydroepiandrostenedione) directly from its intermediate (fetal) zone. In the rhesus monkey, continuous infusion of C19 precursor (androstenedione) leads to preterm delivery [52-54]. This effect is blocked by concurrent infusion of an aromatase inhibitor [54], demonstrating that conversion to estrogen is important in promoting contractions. A similar effect has been shown using a continuous intraamniotic infusion of estrogen [48]. However, systemic infusion of estrogen failed to induce delivery [48], suggesting that the action of estrogen is likely paracrine/autocrine."
Cool, eh?
Oxytocin is also incredibly important, and interestingly concentrations do not increase so much as receptor number does:
"Circulating levels of oxytocin do not change significantly during pregnancy or prior to the onset of labor [55,56]. However, myometrial oxytocin receptor concentrations increase approximately 100 to 200-fold during pregnancy, reaching a maximum during early labor [55,56,58,59]. This rise in receptor concentration accounts for the increased sensitivity of the myometrium to circulating levels of oxytocin during the second half of pregnancy."
Also: "Studies examining fetal pituitary oxytocin production, the umbilical arteriovenous difference in plasma oxytocin concentration, amniotic fluid oxytocin levels, and fetal urinary oxytocin output demonstrate conclusively that the fetus secretes oxytocin into the maternal circulation [55,60]. Furthermore, the calculated oxytocin secretion rates from the fetus suggest an increase from a baseline of 1 mU/min prior to labor to approximately 3 mU/min after spontaneous labor."
Which is cool. They go on to say that oxytocin likely doesn't stimulate labour, but does result in more forceful uterine contractions and increases the likelihood of a successful delivery.
Okay, I'm done nerding out for now. Gonna shower and then walk the dog and
head out to New Sud to see Robyn for lunch.