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At least 343 records · Page 19Linked to original sources
PubMed2004

Labor induces a maternal inflammatory response syndrome.

OBJECTIVE: We studied the effect of labor on maternal neutrophil phenotype. STUDY DESIGN: Neutrophil apoptosis with inflammatory cytokines and the expression of CD11b, CD34 and toll-like receptor 4 (TLR4) were assessed with flow cytometry in women at uncomplicated vaginal delivery (VD), and elective cesarean section (ElCS) without labor, emergency cesarean section with (EmCSL+) or without (EmCSL-) labor. RESULTS: Spontaneous neutrophil apoptosis is delayed in maternal neutrophils after VD, EmCSL+ or EmCSL- versus ElCS. In all groups lipopolysaccharide delayed apoptosis and increased CD11b expression. Elevated TLR4 expression in ElCS was associated with lipopolysaccharide responsiveness. CD34 was diminished in VD, indicating increased cell maturity. CONCLUSION: Normal labor primes the neutrophil and may enhance antibacterial function by inducing a mild maternal inflammatory response syndrome. Delayed neutrophil apoptosis may promote the neutrophilia seen in women after VD. We suggest that labor of any duration may be immunologically beneficial to the parturient.

Antigens, Surface↗
PubMed1994

[The course of induced labor after use of intracervical extra-amniotic prostaglandin F2 alpha in pregnant patients with EPH gestosis].

The aim of our study was to assess the efficacy of labor induction among patients affected by EPH gestosis after intracervical extra-amniotic insertion of 15 mg PGF2 alpha in methyl-cellulose gel. We concluded that PGF2 alpha when given intracervically in methyl-cellulose gel is a highly effective inducer of cervical ripening process as well as subsequent uterine contractions, too. It should be stressed that in no case did we find blood pressure increase after such therapy.

Adult↗
PubMed1985

Plasma levels of 13,14-dihydro-15-keto prostaglandin F2 alpha, estrogens, and progesterone during stretch-induced labor at term.

The uterus of six healthy multiparous women at term was mechanically stretched by a rubber catheter and balloon. Apparent labor was inaugurated in all cases within 5 hours and increased progressively with time. Advanced cervical softening and dilatation were also evident after the stretch treatment. Significant increases in the levels of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) were observed with the progress of treatment (P less than 0.01). Plasma estrogens and progesterone levels did not change significantly during the treatment (P greater than 0.05). Stretching and/or resulting uterine contractions appear to induce the secretion of prostaglandin F2 alpha (PGF) from the organ, which in turn seems to be involved in both cervical softening, and the onset and progress of labor, under stable conditions of plasma estrogens and progesterone.

Adult↗
PubMed1995

[Premature rupture of fetal membranes at term: an indication for induced labor with prostaglandins?].

Premature rupture of membranes (PROM) at term is thought to be related to an increased infection risk for mother and child. A prospective study was conducted to evaluate the efficacy of prostaglandins for induction of labour in 433 cases of PROM presenting after 35 completed weeks of gestation. Intracervical gel or vaginal pessaries were given in dependence on the Bishop-score. Course of delivery and fetal outcome were analysed. In 57.3% single application was sufficient to induce the delivery. Only 1.8% of cases did not respond. 21% of patients were delivered within six hours of the first application and 89.6% during the first 24 hours. The rate of cesarean section was 15.5%. Fetal distress caused by uterine hyperstimulation was observed in 9.9% and required intrapartum tocolysis. A fetal acidosis (pH < 7.15) was present in 4.1%. The neonatal infective morbidity was 0.4%. Severe maternal complications were not observed. We conclude that use of prostaglandins for induction of labour in case of PROM at term seems to be a recommendable measure. In primiparous women or in the presence of an unfavorable cervix-score shorter duration to delivery diminishes the risk of fetal infection.

Administration, Intravaginal↗
PubMed1995

[Randomized comparative study of induced labor with oxytocin and misoprostol in prolonged pregnancies].

UNLABELLED: The efficacy of oxytocin for induction of labor at 41 to 42 weeks of gestational age, was compared with misoprostol (a PGE1 analog) in 100 pregnant women. Half a tablet containing 100 mcg of misoprostol was placed intravaginally in 50 women and the remaining 50 received iv oxytocin (2-32 mU/min). The obstetric features were similar in both groups. Delivery within 24 hours was achieved in 88% of the patients induced with misoprostol and in 72% with oxytocin (p < 0.05). The mean time from induction to delivery was similar, 10.3-10.9 hrs (p NS) and no differences in obstetric and perinatal outcomes were found. Polisystoly with misoprostol, was the only side effect observed in the study (11.4%), and was without neonatal consequences. CONCLUSION: intravaginal misoprostol (100 mcg), is more effective, cheaper and less stressful than IVI oxytocin in post term inductions. The safety profiles of both were similar.

Abortifacient Agents, Nonsteroidal↗
PubMedDate not supplied

Prostaglandin F2 alpha for interrupting pregnancy, managing intrauterine death and molar pregnancy and inducing labor.

Serial intramuscular injections of 250 microgram of 15 (S), 15-methyl-prostaglandin F2 alpha were given to 105 women every 1-3 hours in an attempt to induce second-trimester abortion (N = 80) or labor (N = 25), the latter because of late intrauterine death or anencephaly. The treatment was highly successful; the cumulative expulsion rates at 12 and 24 hours were 69% and 95%, respectively. There were no serious complications, and significant alterations in the mother's vital signs were uncommon. Gastrointestinal side effects are tolerable if the woman is properly premedicated and maintained on the antiemetic, antidiarrheic and analgesic treatments.

Abortion, Induced↗
PubMed2003

Protective effect of N-acetylcysteine against fetal death and preterm labor induced by maternal inflammation.

OBJECTIVE: Intrauterine and maternal systemic infections are proposed causes of preterm labor. The resulting prematurity is associated with 75% of infant mortality and 50% of long-term neurologic handicaps. We hypothesize that free radicals generated in large quantities during an inflammatory response shift the fetomaternal redox balance to an oxidative state, compromising the fetus. Thus, if our working hypothesis is correct, selective inactivation of free radicals with N-acetylcysteine (NAC), an antioxidant and glutathione (GSH) precursor, would improve the outcome of preterm deliveries associated with inflammation. We tested aspects of this hypothesis in an animal model of preterm labor and fetal damage (death). STUDY DESIGN: NAC (1 g/kg) was administered orally to C57Bl/6 mice injected intraperitoneally with either 10 microg lipopolysaccharide (LPS) or saline solution (CRL) on day 16 of gestation. The latency period (time from injection to delivery of the first pup) and fetal viability were recorded. To discriminate between an effect of prematurity from an effect of inflammation, and to document any improvement in survival, mice were killed at 3, 6, and 16 hours after injection. Maternal and fetal redox states were approximated by measuring hepatic GSH. RESULTS: Each C57Bl/6 LPS-treated mouse delivered prematurely after a significantly shorter latency period (LPS: 16.8 hours [95% CI 15.9-17.6] vs CRL: 54.7 hours [95% CI 43.8-65.5]). NAC doubled the latency interval of LPS-treated animals to 35.2 hours (95% CI 21.0-49.2). LPS alone resulted in a 100% rate of stillbirth. Fifty-eight percent of fetuses were already dead 16 hours after LPS. In contrast, only 33% of fetuses were dead 16 hours after LPS (P =.001) when NAC was given. LPS was followed by a reduction in maternal (LPS: 26.3 nmol/mg [95% CI 19.9-32.8] vs CRL: 41.3 nmol/mg [95% CI 34.7-47.9, P <.01]) and fetal GSH (LPS: 19.7 nmol/mg [95% CI 11.7-27.8] vs CRL: 34.5 nmol/mg [95% CI 32.0-37.0, P <.001]). This decline was reversed by NAC (NAC/LPS maternal GSH: 37.0 nmol/mg [95% CI 22.5-51.5] and fetal GSH: 28.4 nmol/mg [95% CI 22.8-33.9]). Importantly, maternal liver GSH impacted on fetal survival. NAC/LPS mothers with living pups 16 hours after LPS had significantly higher liver GSH compared with NAC/LPS mothers whose pups died in utero. In fact, all NAC-treated mice whose hepatic GSH exceeded 20 nmol/mg had living fetuses at 16 hours. CONCLUSION: Maternal inflammation in C57Bl/6 mice results in oxidative stress associated with maternal and fetal GSH depletion. Oxidative stress damages the fetus independent of prematurity. Restoration of maternal and fetal oxidative balance by NAC protects the fetus and reduces the rate of preterm birth.

Acetylcysteine↗
PubMed2004

Effect of proteasome pathway on initiation of mouse labor induced by antiprogesterone.

PROBLEM: Various kinds of contraction-associated molecules are up-regulated at the initiation of labor. However, expression profiling has revealed that many molecules are also down-regulated. The effect of down-regulation of molecules by protein degradation on parturition is not known. METHODS OF STUDY: We administered lactacystin, a specific proteasome inhibitor, to mouse preterm birth model induced by antiprogesterone RU486 on day 16.0 post-coitus. NF-kappaB activity, and the levels of transcripts for oxytocin receptor, prostaglandin F(2alpha) receptor (FP), cyclooxygenase-1, -2, and interleukin-1beta in the uterus were examined by electrophoretic mobility shift assay and semi-quantitative reverse transcriptase-polymerase chain reaction, respectively. RESULTS: Administration of lactacystin significantly prolonged the time until the delivery of the first pup. FP mRNA level was solely elevated by RU486 treatment, and lactacystin significantly suppressed this up-regulation. CONCLUSIONS: Proteolysis by proteasomes in the uterus regulates the initiation of labor, at least in part, via control of contraction-associated molecules such as FP.

Abortifacient Agents, Steroidal↗
PubMed1980

Changes in serum hormone levels during labor induced by oral PGE2 or oxytocin infusion.

The hormonal changes in maternal serum during parturition induced by amniotomy and oxytocin (OXY) infusion or oral prostaglandin E2 (PGE2) medication have been compared in 68 patients (33 women in the PGE2 group, 35 in the oxytocin group). The effect of PGE2 differed from that of oxytocin. Thus the prostaglandin elicited increases in total estriol (p < 0.001) and decreases in prolactin (p < 0.01), TSH (p < 0.05) and HPL (p < 0.05) from the basal level to that immediately before parturition. Maternal serum cortisol levels rose to the same extent in both treatment groups (p < 0.001). The significant (p < 0.05) increase occurred earlier among women receiving PGE2 (two hours into therapy), even though labor pain was experienced later in this group. The serum estriol elevation in these patients was significant three hours after start of therapy (p < 0.05). A similar time course was noted for the decrease of serum prolactin in PGE2 treated patients. The drop in maternal serum levels of HPL and TSH in the PGE2 group was significant only immediately prior to partus. Neither PGE2 nor oxytocin induced changes in maternal serum levels of HCG or alpha-fetoprotein or estradiol. Oxytocin but not PGE2 lead to a decrease in maternal serum progesterone concentrations; this was significant (p < 0.05--p < 0.01) only late in labor. Mixed umbilical serum levels of the hormones mentioned above were the same regardless of method of induction. Hence the increased maternal estriol concentrations during PGE2 treatment were not reflected in fetal blood. It is suggested that increases in maternal estriol levels during PGE2 medication are due to effects on the maternal enterohepatic circulation rather than on the fetoplacental unit. Irrespective of maternal treatment umbilical serum from female newborns contained statistically higher (p < 0.05) levels of estradiol and HCG than serum from male children.

Administration, Oral↗
PubMed2006

Uterine transcriptomes of bacteria-induced and ovariectomy-induced preterm labor in mice are characterized by differential expression of arachidonate metabolism genes.

OBJECTIVE: The purpose of this study was to identify changes in gene expression that are associated with preterm labor induced by either bacteria or ovariectomy. STUDY DESIGN: Pregnant mice (14.5 days of gestation) were allocated to: (1) intrauterine injection of heat-inactivated Escherichia coli; (2) media alone; (3) ovariectomy; or (4) sham operation. The uterine transcriptome was studied with photolithographic, very short oligonucleotide-based microarrays, and arachidonate metabolism genes were assayed with quantitative reverse transcriptase-polymerase chain reaction. Significance was determined by analysis of variance. RESULTS: Microarray-based gene expression changes in the arachidonate metabolism pathway are associated globally with bacteria-induced preterm labor (P < or = .0031) and ovariectomy-induced preterm labor (P < or = .00036). Quantitative real-time reverse transcriptase-polymerase chain reaction measurements demonstrated that bacteria-induced preterm labor substantially increased the expression of genes involved in prostaglandin synthesis. In contrast, ovariectomy-induced preterm labor increased the expression of genes involved in lipoxin, leukotriene, and hydroxyeicosatetraenoic acid synthesis. CONCLUSION: Bacteria-induced and ovariectomy-induced preterm labor each express a different balance of genes that are required for the synthesis of prostaglandins, lipoxins, leukotrienes, and hydroxyeicosatetraenoic acids.

Animals↗