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Cervix stretches...uterus contracts...
Pregnant women: OBs are closing birth canals up to 30%.
It's easy to allow your birth canal to OPEN the "extra" up to 30%.
See the very end of this post...
CERVIX STRETCHES...UTERUS CONTRACTS...
THE FETUS-EJECTION REFLEX...
"DILATATION (STRETCHING) OF THE CERVIX AUGMENTS UTERINE ACTIVITY BY
AUGMENTING OXYTOCIN SECRETION..."
DR. JAMES FERGUSON
James K. W. Ferguson's career parallels and reflects the history of the
Banting Research Foundation and the development of medical research in
Canada. The story begins in 1929 when as a young graduate student in
physiology at the University of Toronto he first met Dr Charles Best, who at
age twenty-nine had just been appointed Professor and head of the
department...In 1940 Ferguson established the hormonal basis of a major
reflex controlling childbirth. As early as 1932, his final year of medical
school, he had wondered whether there was a connection between the
contractions of labour and "the posterior pituitary hormone, oxytocin" for
which no function had yet been discovered. During his two-year assistant
professorship at Ohio State University between 1936 and 1938, Ferguson and
endocrinologist Hans Haterius found that electrical stimulation of the
pituitary gland of anaesthetized rabbits produced "definite, and at times
enormous" increases in uterine activity. Ferguson continued this research
after his appointment to the pharmacology department at Toronto in 1938, and
two years later successfully demonstrated that dilatation (stretching) of
the cervix augments uterine activity by augmenting oxytocin secretion. This
discovery, which became known as Ferguson's reflex, has important
implications for the management of tabour as the use of epidural
anaesthetics interferes with this reflex, resulting in longer labours and an
increased incidence of forceps delivery.
IN RATS: "THE FETUS-EXPULSION REFLEX DIFFERS FROM THE FETUS-EJECTION
Exp Neurol. 1987 May;96(2):443-55. PubMed abstract
Pelvic neurectomy abolishes the fetus-expulsion reflex and induces dystocia
in the rat.
Higuchi T, Uchide K, Honda K, Negoro H.
To clarify the origin of dystocia in bilaterally pelvic neurectomized (BPN)
rats, the uterine activity during the periparturient period, and reflex
straining movements in response to vaginal stimulation and cervical
extensibility were monitored. The BPN rat displayed "stretching" movements
and the regular continuous uterine activity with a similar onset and
intensity to that in control rats (intact, sham-operated or unilateral
pelvic neurectomized rats) on days 22 or 23 of gestation, but lacked the
"straining" movements which precede each delivery of pups in controls so
that parturition was prolonged. Dissection of rats revealed that an unborn
fetus was retained in the expanded upper portion of the vaginal cavity.
Vaginal distension induced contraction of the abdominal muscles and
diaphragm and an inhibition of respiratory movements, resulting in an
increase in intraabdominal pressure in urethane-anesthetized control rats.
This reflex muscular contraction which reflects the straining movements in
normal delivery may be called the fetus-expulsion reflex and does not occur
in BPN rats. It differs from the fetus-ejection reflex (Ferguson reflex)
which initiates oxytocin release. There was no difference in weight and
distensibility of the uterine cervix between sham-operated and operated rats
on day 22 of pregnancy. The results suggest that the main abnormality of
delivery in BPN rats, a prolongation of the process of delivery, may be due
to a lack of the fetus-expulsion reflex which plays a physiologic role in
removing a fetus from the upper vaginal cavity against the resistance of the
"THE PARADOXICAL OXYTOCIC EFFECT OF ADRENALINE"
Midwifery Today Int Midwife. 2003 Fall;(67):20-2. PubMed abstract
Fear of death during labour.
The expression of fear of death during labour is common when the
physiological processes are obviously efficient and when the perinatal
period is considered, in retrospect, to have been a positive experience. We
propose two kinds of interpretation: (1) One is not specifically human. A
physiological fear is the expression of a rush of adrenaline just before the
"fetus ejection reflex." The paradoxical oxytocic effect of adrenaline was
demonstrated several decades ago. (2) One is specifically human. It takes
into account our knowledge of death and the reduction of neocortical control
IN CATS? "THE NUCLEUS TRACTUS SOLITARII (NTS) [RELAYS AFFERENT STIMULI
ARISING FROM THE BIRTH CANAL]...TO THE OXYTOCIN NEURONES..."
Adv Exp Med Biol. 1995;395:95-104. PubMed abstract
Opioid-noradrenergic interactions in the control of oxytocin cells.
Leng G, Brown CH, Murphy NP, Onaka T, Russell JA.
Department of Physiology, University Medical School, Edinburgh, UK.
The nucleus tractus solitarii (NTS) projects directly to the oxytocin
neurones of the supraoptic nucleus (SON), and relays afferent stimuli
arising from the birth canal during parturition. About 80% of these
projecting neurones are noradrenergic, and these same neurones are activated
following systemic administration of cholecystokinin (CCK), which also
results in an increased electrical and secretory activity in oxytocin
neurones. Oxytocin release in response to CCK is abolished following
selective neurotoxic destruction of these noradrenergic neurones. Oxytocin
release following CCK (and that during parturition) is potently inhibited by
morphine, which blocks the local noradrenaline release in the supraoptic
nucleus. This acute opiate action involves presynaptic inhibition of the
noradrenergic terminals, and occurs without marked suppression of the
activity of noradrenergic cells in the NTS. During chronic exposure to
morphine the oxytocin system becomes tolerant to, and dependent upon
morphine. In the course of tolerance, oxytocin cell activation in response
to CCK recovers from initial inhibition. However, the pathway that mediates
this response does not appear to become dependent: the oxytocin cell
response to CCK is unchanged by opiate withdrawal induced by naloxone,
despite a large increase in the background electrical activity of oxytocin
cells provoked by withdrawal. Nevertheless, expression of withdrawal
excitation by oxytocin neurones is curiously contingent upon the activity of
the noradrenergic input in that prior lesioning of this input has no effect
upon the subsequent withdrawal excitation of oxytocin cells. Yet under
urethane anaesthesia, acute pharmacological blockade of the noradrenergic
input suppresses withdrawal. We discuss how these paradoxical observations
might be reconciled, and note that the difference may be related to
differing levels of tonic activity in the noradrenergic input. It is
possible that dependence relies upon the input when it is there, but not
when it is not.
1986: "OXYTOCIN HAS RECENTLY BEEN IDENTIFIED IN THE ADRENAL MEDULLA..."
Regul Pept. 1986 Apr;14(2):125-32. PubMed abstract
Oxytocin inhibits ACTH and peripheral catecholamine secretion in the
Oxytocin (OT) generally has a stimulatory effect on ACTH secretion both in
vitro and in vivo. As part of a study of ACTH-releasing factors in
hypophysial portal blood, the effects of i.v. OT administration on plasma
ACTH levels were tested in urethane-anesthetized rats. Surprisingly, i.v.
injection of 10 micrograms OT lowered plasma ACTH levels by about 35% (P
less than 0.01). It was reasoned that this paradoxical inhibition of ACTH
secretion by OT might be mediated by inhibition of the unusually high rate
of peripheral catecholamine secretion in this model. Measurement of plasma
catecholamines before and after i.v. administration of 10 micrograms OT
revealed a 53% inhibition of EPI (P less than 0.01) and 43% inhibition of NE
(P less than 0.05). Administration of the beta-adrenergic antagonist
propranolol (400 micrograms) 15 min before the beginning of the experiment
completely blocked the inhibitory effects of OT on ACTH secretion and in
fact unmasked the stimulatory effects of OT normally seen in conscious
animals and in vitro. Superfused bisected adrenal glands exposed to 10(-6) M
OT for 10 min secreted more than 30% less EPI and NE than control adrenals
suggesting that the inhibition of EPI and NE secretion by OT in vivo occurs,
at least in part, directly at the level of the adrenal. The data support the
hypothesis that peripheral catecholamines may at times be directly involved
in the control of ACTH secretion and also suggest that OT, which has
recently been identified in the adrenal medulla, may have important
paracrine functions in the regulation of adrenal catecholamine secretion.
Years ago, Michel Odent, MD told me that, as part of the fetus-ejection
reflex women who labor feeling unobserved will spontaneously get off their
Of course, getting off the sacrum allows the birth canal to open an "extra"
up to 30%...
WARNING: The two most common medical delivery positions - semisitting and
dorsal - keep the woman on her sacrum/close the birth canal the "extra" up
WORSE: When babies get stuck, OBs routinely KEEP the birth canal closed the
"extra" up to 30% - i.e. - they keep women semisitting or dorsal as they
pull with forceps.
PREGNANT WOMEN: To allow the birth canal to OPEN the "extra" up to 30% -
roll onto your side as you push your baby out. Beware though: Some OBs
will let women "try" alternative delivery positions but will put them
semisitting or dorsal (close the birth canal the "extra" up to 30%) for the
Women shouldn't have to ask for the "extra" up to 30% - but that's the way
it is - so talk to your OB today.
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