OBJECTIVE: To evaluate the incidence of respiratory distress syndrome (RDS) in infants born to mothers with placenta previa and to assess the risk factors for RDS. METHODS: Ninety-nine pregnant women with placenta previa who delivered by cesarean section at 30-35 weeks of gestation were compared retrospectively with 102 pregnant women matched for week of gestation and birth year, who underwent elective cesarean section. Maternal characteristics, neonatal outcome, and incidence of RDS were analyzed. Umbilical cord blood samples were collected at delivery and were used to determine cortisol, epinephrine, and norepinephrine levels. Student's t-test, the chi-square test, and Fisher's exact test were used for statistical comparisons. P < 0.05 was considered significant. The Mann-Whitney U test was used for comparison of continuous variables. RESULTS: Preeclampsia, histological chorioamnionitis, and premature rupture of membranes were significantly lower in the placenta previa group (placenta previa: 2.0% vs. control: 14.7%, P < 0.01; 14.1% vs. 30.1%, P < 0.01; 7.1% vs. 17.6%, P < 0.05, respectively). The incidence of RDS was significantly higher in the placenta previa group than in the control group (29.3% vs. 6.9%, P < 0.0001). The cortisol level in umbilical cord blood in the placenta previa group was lower than in the control group (median 7.3, range 4.4-14.9 microg/dl vs. median 10.6, range 4.9-30.3 microg/dl, P < 0.05). There were no significant differences in epinephrine or norepinephrine levels between the two groups. CONCLUSIONS: The incidence of RDS in infants delivered at 30-35 weeks' gestation by cesarean section was significantly higher in mothers with placenta previa than in women without placenta previa. This may reflect decreased fetal stress since the cord blood cortisol levels were found to be lower in women with placenta previa.

Cesarean Section↗

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Estrogen induced enhancement of LHRH clearance in amenorrheic women.

In order to assess the effect of estrogen administration on LHRH metabolism in human plasma, plasma LHRH levels were determined in six amenorrheic women following iv injection of 500 ng synthetic LHRH before and after im injection of 5 mg estradiol benzoate (EB) for 4 days. The plasma levels of LHRH reached a maximum 1.25 min after LHRH administration, and they rapidly decreased in both situations. The initial disappearance of LHRH after EB treatment (half-life = 1.87 +/- 0.15 min) was significantly (p less than 0.05) more rapid than that before treatment (half-life = 2.45 +/- 0.21 min). The mean basal levels of plasma estradiol significantly (p less than 0.05) increased from 15.2 pg/ml to 4,387 pg/ml after EB treatment. Gonadotropin response to LHRH after EB treatment were not different from those before treatment. These data suggest that exogenous estrogen may stimulate the clearance of LHRH from the plasma of amenorrheic women.

Adult↗

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The mechanism of the effect of combination treatment with clomiphene and bromocriptine in patients with normoprolactinemic anovulation.

The combination treatment with bromocriptine and clomiphene citrate was applied to 11 normoprolactinemic anovulatory patients who did not respond to clomiphene citrate alone. This combination treatment restored ovulation in 8 of these patients (72.7%). Conception was observed in 2 patients (18.1%) out of 11. The patients who responded to combination treatment showed a significant increase in the serum level of estradiol in the preovulatory phase, of progesterone in the mid-luteal phase, and a significant decrease of serum prolactin. They also showed significant increase in the frequency of luteinizing hormone (LH) pulsatility on day 12 of the cycle from 1.38 +/- 0.86 to 3.75 +/- 0.83 pulses/4h. The 3 patients who did not respond to combination treatment showed no increase in the serum level of estradiol or progesterone, but showed increase in the frequency of LH pulsatility in spite of continuous anovulation. These results indicate that the combination treatment with bromocriptine and clomiphene citrate is effective for treatment of patients with normoprolactinemic anovulation who do not respond to clomiphene alone, and suggest that the mechanism of the effect of combination treatment is related to an increase in the frequency of LH pulsatility caused by bromocriptine, which in turn stimulates follicular maturation.

Adolescent↗

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Spontaneous pregnancy after a pregnancy induced by treatment in hyperprolactinemic women.

The relationship between spontaneous pregnancy of hyperprolactinemic patients after a first pregnancy induced by treatment and their serum prolactin levels was examined. Of the 100 patients with hyperprolactinemia studied, 74 became pregnant after treatment; namely, 20 transsphenoidal adenomoidectomy for pituitary prolactinoma (group 1), 26 on treatment with bromocriptine for pituitary prolactinoma (group 2), and 28 on treatment with bromocriptine for hyperprolactinemia without prolactinoma (group 3). After delivery in the first pregnancy, the rates of menstrual restoration and subsequent spontaneous pregnancy in group 1 (72.2% and 75.0%) were significantly (p less than 0.05) higher than those in group 2 (32.0% and 25%) and group 3 (13.6% and 18.2%). The serum levels of prolactin after the first pregnancy and weaning were significantly (p less than 0.05) lower in patients with subsequent spontaneous pregnancy than in patients without spontaneous pregnancy in each group, and the levels in patients with spontaneous pregnancy were significantly (p less than 0.05) lower in group 1 (15.2 +/- 8.8 ng/ml) than in group 2 (46.6 +/- 2.9 ng/ml). These data suggest that the transsphenoidal adenomoidectomy for pituitary prolactinoma may be better than bromocriptine treatment for recovery of reproductive function.

Adult↗

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Specific cytotoxicity of antibody to YAL-198, a sperm antigen peptide, to murine zygote.

Active immunization with the peptide segments rSMP-230 and YAL-198, corresponding to the hydrophilic extracellular domain of two human sperm antigens (rSMP-B and YWK-II, respectively), reduced fertility in female rats by different mechanisms. The anti-rSMP-230 antibody interferes with human and murine fertilization, and the anti-YAL-198 antibody blocks the development of mouse embryos. The authors examined in vitro at which stage the antibodies to rSMP-230 and YAL-198 were cytotoxic to murine embryos up to morula/blastocyst stage. Anti-rSMP-230 antibody was not cytotoxic to any stages. On the other hand, the anti-YAL-198 antibody arrested the growth of embryos at the 2-cell stage but not at more advanced developmental stages. When the anti-YAL-198 antibody was used, spotty staining was observed only on the surfaces of embryos that had arrested at the 2-cell stage. Unstained embryos, however, continued to develop normally. In contrast, the anti-rSMP-230 antibody stained murine sperm but failed to stain murine ova and embryos. The present results suggest that the human sperm components rSMP-B and YWK-II play important roles in sperm-egg interaction and early development of the embryo, respectively.

Animals↗

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Progesterone accelerates the onset of capacitation in mouse sperm via T-type calcium channels.

This study was undertaken to evaluate whether progesterone induces capacitation of mouse spermatozoa. When sperm were evaluated by chlortetracycline staining, addition of progesterone significantly increased the proportion of spermatozoa exhibiting the B pattern at 60 minutes of incubation, compared with that before incubation (23 +/- 6.2% vs. 13 +/- 2.9%, p < 0.01) and that in hTF medium without progesterone (23 +/- 6.2% vs. 13 +/- 4.2%, p < 0.01). If the redistribution of proteins in sperm plasma membrane such as protein binding calcium ion were defined as capacitation, it could be said that progesterone promoted capacitation of mouse sperm. This progesterone-induced capacitation was prevented by depletion of extracellular calcium ion and addition of NiCl2, a T-type calcium channel blocker, although thapsigargin, an inhibitor of Ca2+-ATPase, did not increase the number of capacitated sperm (B pattern; progesterone vs. progesterone + depletion of calcium ion, 18 +/- 3.5% vs. 8 +/- 2.5%, p < 0.05, progesterone vs. progesterone + NiCl2, 20 +/- 3.8% vs. 6 +/- 5.2%, p < 01). Furthermore, genistein, a protein tyrosine phosphorylation inhibitor, inhibited progesterone-induced capacitation (B pattern; progesterone vs. progesterone + genistein, 20 +/- 3.8% vs. 11 +/- 2.4%, p < 01). In conclusion, progesterone induces capacitation in mouse sperm and this capacitation may be associated with calcium influx and tyrosine phosphorylation.

Animals↗

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Sperm-immobilizing antibodies block capacitation in human spermatozoa.

Sperm-immobilizing antibodies block human fertilization by interfering with the acrosome reaction (AR). To clarify the mechanism of blockage of AR by sperm-immobilizing antibodies, the authors examined their effects on the increase of intracellular free Ca2+ concentration induced by follicular fluids (Ca2+ influx) in spermatozoa and on their capacitation. Sperm-immobilizing antibodies did not suppress Ca2+ influx induced by follicular fluid, but they inhibited capacitation of human spermatozoa. Namely delta%AR (%AR after addition of an AR inducer--%AR before treatment) induced by progesterone was significantly (p < .0001) lower when spermatozoa were incubated in human tubal fluid medium cotaining antibody-positive serum (1.2%), compared to that when incubated in control medium (19.2%). Furthermore, the proportion of both spermatozoa that became capacitated and ones that had become capacitated decreased significantly (p < .0001) after 2, 4, and 6 h of incubation in medium containing antisperm antibody-positive serum, compared to those of spermatozoa incubated in control medium. In conclusion, sperm-immobilizing antibodies may be closely related to their blockage of capacitation.

Acrosome Reaction↗

PubMedDate not supplied

Concentration of granulocyte elastase in seminal plasma is not associated with sperm motility.

Although elastase could affect sperm motility in vitro, secretory leukocytes protease inhibitor (SLPI) prevents sperm from being attacked by elastase. The authors investigated the correlations of elastase level with sperm motility and SLPI level in vivo. Semen samples (n = 116) were collected and centrifuged after semen analysis. Elastase and SLPI levels were determined by an enzyme immunosorbent assay. Samples were classified by elastase levels into low (<250 ng/mL), moderate (250-1,000 ng/mL), and high elastase groups (> or =1,000 ng/mL). Elastase levels (range, 2.8-23,974.4 ng/mL) were not associated with sperm motility. The median SLPI level in the high elastase group was 15,900 ng/mL (range, 2.860-46,900 ng/mL). However, there was no significant correlation between elastase and SLPI levels in seminal plasma. Since SLPI forms a 1:1 complex with elastase, these results suggest that seminal plasma has a sufficient amount of SLPI to protect spermatozoa from elastase.

Enzyme Inhibitors↗