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OBJECTIVE: Human myometrium contains both beta1-adrenergic and beta2-adrenergic receptors. This study was designed to assess the importance of each beta-adrenergic receptor subtype in relaxation of human myometrial muscle strips. STUDY DESIGN: Radioligand binding studies were used to establish the presence of each beta-adrenergic receptor subtype, whereas highly selective beta1-antagonists and beta2-antagonists were used to assess the contribution of beta-adrenergic receptor subtypes to myometrial relaxation after exposure to (-)-isoproterenol. RESULTS: Membranes prepared from myometrium contained 82% +/- 4% beta2-adrenergic receptors. After contraction produced by exposure to potassium chloride (35 mmol/L), isoproterenol produced relaxation with half maximal effect at 0.02 micromol/L and a maximal relaxation of 52% +/- 3%. Beta1-antagonist CGP-20712A had no significant effect, whereas beta2-antagonist ICI-118551 produced a characteristic rightward shift of the isoproterenol concentration-relaxation relationship. CONCLUSIONS: Although both beta1-adrenergic receptors and beta2-adrenergic receptors are present in human myometrial tissue at term, relaxation by nonselective beta-agonist isoproterenol is mediated exclusively by beta2-adrenergic receptors.

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Leukocyte beta 2-adrenoceptors mirror similar receptors in the uterus. This study examined changes in beta 2-adrenoceptors and in cAMP production during pregnancy using peripheral mononuclear leukocytes isolated from 17 pregnant women and 5 nonpregnant controls. beta 2-Adrenoceptor density was determined by 125I-pindolol binding. cAMP production under basal and stimulated (10 microM isoproterenol) conditions was determined by radioimmunoassay. Groups were compared by unpaired t test. There was a nonsignificant decrease in the density of beta-adrenoceptors during pregnancy. While basal cAMP production was unchanged during pregnancy, stimulated cAMP production was decreased (44% of control, P < 0.001; 95% CI 33%-56%). Stimulated cAMP production per receptor was lower in leukocytes from pregnant women and was not a constant relationship, but was increased markedly in leukocytes having fewer than 400 beta-adrenoceptor sites per cell. There are significant changes in the coupling of beta-adrenoceptors to cAMP production during pregnancy without changes in beta-receptor density, affinity, or basal cAMP production.

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A 15-year-old primigravida registered late for antenatal care (23 weeks). Ultrasound examination revealed massive idiopathic fetal ascites necessitating in utero paracentesis at 27 weeks. The family was socially dislocated, and the patient's alcoholic father doted on her. A live female fetus with ascites and multiple congenital abnormalities was delivered at 34 weeks. Following repeated hospitalization, the infant died of pneumonitis, at 5 months of age; autopsy could not determine the cause of the ascites. Young pregnant teenagers from broken homes with doting behavior from an alcoholic father should be suspected of being incest victims.

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Incarceration and sacculation of a retroflexed gravid uterus is relatively benign, in contrast with pregnancy in a rudimentary uterine horn which can lead to perforation and hemorrhage. We report a case of pregnancy in an incarcerated sacculated non-communicating rudimentary horn mimicking incarceration with sacculation of a retroflexed gravid uterus. Both physical and sonographic findings were unhelpful in the differential diagnosis. Therefore, decision for laparotomy in such cases should be based on severity of symptoms.

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Plasma 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine concentrations were measured in fetal sheep prior to death in utero and after thyroidectomy. In six fetal sheep who subsequently died in utero, plasma rT3 concentrations were elevated in all for 2 to 13 days prior to death. There were no consistent changes in plasma T4 concentrations. In two thyroidectomized fetal sheep, plasma T4 and rT3 concentrations fell to low levels. Plasma T3 concentrations remained low and there was no increase in plasma T3 in the last week prior to parturition like that which occurs in normal fetal sheep. Parturition was preceded by the normal increase in fetal plasma cortisol concentrations and occurred at the normal time. These data indicate that plasma rT3 concentrations are increased as a result of illness in fetal sheep and that such measurements may be useful as an indicator of fetal distress. The normal increase in plasma T3 late in gestation is not necessary for the late gestational cortisol surge or for normal parturition.

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Plasma thyroid hormone and cortisol concentrations were measured from early third trimester to delivery in seven pregnant ewes and their fetuses. A surge in fetal plasma triiodothyronine was found during the six days prior to delivery, the mean values rising from less than 30 to 125 ng. per deciliter. During this period the fetal plasma cortisol also increased from less than 1 to 8.1 microgram per deciliter. During this period there was no significant change in fetal plasma thyroxine (T4) or reverse T3 concentrations and no change in maternal plasma concentrations of any of these hormones. The abrupt increase in fetal plasma T3 concentrations with no rise in plasma T4 suggests that there was an alteration in extrathyroidal conversion of T4 to T3 rather than an increase in thyroid secretion, since the latter would be expected to cause an increase in both plasma T4 and plasma T3. The changes in plasma T3 and cortisol concentrations in a fetus that died in utero eight to 10 days before term resembled those occurring prior to normal parturition.

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Diminished total plasma cortisol levels have been demonstrated in postmature neonates, suggesting that fetal glucocorticoids may be involved in the cause of postmaturity. This hypothesis was tested by adrenocortical stimulation in 32 newborns: 12 were postmature; 12 were postterm, but not postmature; and 8 were normal term neonates. The mean pre- and poststimulation total plasma cortisol levels were 3.9 and 50.9 microgram/100 ml, respectively, for the postmature newborns, 9.7 and 44.0 microgram/100 ml for the postterm, but nonpostmature newborns, and 9.8 and 37.1 microgram/100 ml for the normal term newborns. The differences in the poststimulation rise in plasma cortisol between the postmature and merely postterm infants or between the postterm and normal term infants were not statistically significant. The mean poststimulation cortisol rise in the postmature group exceeded that of the normal term group (P less than 0.05). The adequacy and promptness of response to adrenocortical stimulation eliminate the likelihood of adrenal insufficiency in postmature infants.

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Amniotic fluid cortisol concentration was measured in 61 gravidas during the third trimester prior to onset of labor. These patients had had normal prenatal courses and served as controls. Cortisol values obtained were compared with those of 1) gravidas with prolonged pregnancy (greater than 42 weeks) who delivered post-mature neonates (N=6), 2) gravidas in spontaneous term labor (N = 10), and 3) gravidas in premature labor (N=10). The mean level of amniotic fluid cortisol (+/-SD) found in those women with premature labor was significantly elevated compared to control values (P less than 0.05). Levels recorded in premature labor patients were in the same range as in the term spontaneous labor group (3.7+/-2.5 vs. 2.7+/-1.5; P greater than 0.3). No difference was found between the spontaneous labor group or the postmature group and their respective controls.

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The fetal adrenal cortex has recently been implicated in the etiology of postmaturity on the basis of low cortisol levels found in the plasma of postmature neonates. These findings suggested that labor could be initiated in prolonged pregnancy by iatrogenic elevation of fetal plasma cortisol. In the current investigation designed to test this hypothesis, 500 mg of hydrocortisone sodium succinate, dissolved in the accompanying diluent of bacteriostatic water to form 4 ml of solution, was injected intraamniotically in 10 patients with unfavorable cervices who were 12 or more days past their expected date of confinement. Nine similar patients serving as controls received 4 ml of bacteriostatic water intraamniotically. All patients were followed with daily determinations of urinary estriol. Eight of the 10 patients who received cortisol went into labor within 120 hours of instillation, as compared with 2 of the 9 patients in the control group. Comparison of the two groups revealed a significant difference (p less than 0.01). The mean instillation-labor time for the cortisol group was 86 hours compared with 228 hours in the control group. This difference was also significant (p less than 0.001). Urinary estriol excretion declined sequentially following cortisol but not after infusion of water. These findings are consistent with the hypotheses that a) spontaneous labor in the human may be preceded by a sudden rise in fetal plasma cortisol, as in the sheep; b) the fetal pituitary-hypothalamic axis is responsive to cortisol, hence the falling estriol excretion; and c) ACTH may be the tropic hormone for the provisional zone of the fetal adrenal cortex.

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Total maternal plasma cortisol levels were measured by a radioassay method in 9 patients who were in spontaneous labor and 10 patients who were electively induced at term with oxytocin. Determinations were made at onset of labor and repeated at full cervical dilatation. Total maternal plasma cortisol levels were also measured in 7 patients undergoing elective cesarean section without labor, determinations being made just prior to the procedure and at the time of uterine incision. Computerized analysis showed the mean initial cortisol level (+/- SE) in the spontaneous labor group (15.4 +/- 1.6 mug/100 ml) to be significantly less than the mean initial level of the group electively delivered by oxytocin induction (37.2 +/- 6 mug/100 ml), with P less than 0.01. The former value was also found to be significantly less than that of the group electively delivered by cesarean section (32.1 +/- 9.3 mug/100 ml), with P less than 0.05. A significant rise was noted at full cervical dilatation in the spontaneous labor group (P less than 0.05), whereas no change occurred in the two elective groups. No significant correlation was found between the maternal cortisol levels on the one hand and the cord cortisol levels. These findings indicate that a) maternal participation is unlikely in bringing about a surge of fetal plasma cortisol which is thought to precede spontaneous labor, b) elective termination of term pregnancy by oxytocin induction or cesarean section may be initially more stress-provoking to the mother than spontaneous labor, and c) maternal stress as measured by plasma cortisol level is not reflected in the fetus.

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Total plasma cortisol in cord and neonatal blood was measured by a radioassay method in neonates resulting from (1) term vaginal delivery following uncomplicated labor (control group), (2) term vaginal delivery following fetal distress during labor, (3) postterm, postmature vaginal delivery following fetal distress during labor, and (4) postterm, postmature emergency cesarean section performed because of signs of severe fetal distress during labor. Comparison of the mean peripheral plasma cortisol values showed that whereas the mean level (plus or minus S.E.) of the distressed term neonates (22.2 plus or minus 5.3 mug per 100 ml.) use 180 per cent of that of the control group (12.3 plus or minus 1.1 mug per 100 ml.; P smaller than 0.01) the mean level for the vaginally delivered postmature group (7.5 plus or minus 1.8 mug per 100 ml.) was only 61 per cent of that of the control group (P smaller than 0.05). Furthermore, in the postmature group with sufficient intrapartum distress to warrant emergency cesarean section the mean level (4.6 plus or minus 1.5 mug per 100 ml.) was found to be only 37 per cent of that of the control group. No differences were observed among the cord plasma cortisol values. These results are strongly suggestive of a relative adrenocortical insufficiency in postmature neonates. Such insufficiency could result from a defect in any portion of the adrenal-pituitary-hypothalamic axis. Effort is under way to further define such a defect.

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