Pharmacokinetics of ethanol and its metabolite, acetaldehyde, and fetolethality in the third-trimester pregnant guinea pig for oral administration of acute, multiple-dose ethanol

1986 ◽  
Vol 64 (8) ◽  
pp. 1060-1067 ◽  
Author(s):  
David W. Clarke ◽  
Nancy A. E. Steenaart ◽  
Christopher J. Slack ◽  
James F. Brien

The pharmacokinetics of ethanol and its metabolite, acetaldehyde, were determined in the third-trimester pregnant guinea pig (56–59 days gestation) for oral intubation of four doses of 1 g ethanol/kg maternal body weight, administered at 1-h intervals. Animals (n = 4–7) were sacrificed at each of selected times during the 26-h study. Ethanol and acetaldehyde concentrations were determined by headspace gas-liquid chromatography. The maternal and fetal blood ethanol concentration–time curves were virtually superimposable, which indicated unimpeded bidirectional placental transfer of ethanol in the matemal–fetal unit. The blood and brain ethanol concentrations were similar in each of the maternal and fetal compartments during the study, which indicated rapid equilibrium distribution of ethanol. There was accumulation of ethanol in the amniotic fluid resulting in higher ethanol concentration compared with maternal and fetal blood during the elimination phase, which indicated that the amniotic fluid may serve as a reservoir for ethanol in utero. Acetaldehyde was measurable in all the biological fluids and tissues at concentrations that were at least 1000-fold less than the respective ethanol concentrations and were variable. There was ethanol-induced fetolethality that was delayed and variable among animals, and was 55% at 23 h. At this time interval, the ethanol concentrations in maternal blood and brain, fetal brain, and amniotic fluid were 35- to 53-fold greater and the acetaldehyde concentrations in maternal blood and fetal brain were four- to five-fold higher in the animals with dead fetuses compared with the guinea pigs with live litters. These data indicated that decreased ethanol elimination from the maternal–fetal unit was related temporally to the fetolethality.

1985 ◽  
Vol 152 (5) ◽  
pp. 583-590 ◽  
Author(s):  
James F. Brien ◽  
David W. Clarke ◽  
Bryan Richardson ◽  
John Patrick

1996 ◽  
Vol 30 (11) ◽  
pp. 1249-1251 ◽  
Author(s):  
Maria L Santeiro ◽  
Carine Stromquist ◽  
Lance Wyble

OBJECTIVE: To report phenoxybenzamine placental transfer in the treatment of maternal hypertension secondary to pheochromocytoma. CASE SUMMARY: A 22-year-old woman diagnosed with pheochromocytoma was medically managed at 33 weeks gestation with oral phenoxybenzamine and labetalol until delivery 26 days later. To determine phenoxybenzamine placental passage, at the time of cesarean section simultaneous samples were obtained from the cord blood, maternal blood, and amniotic fluid. Additional blood samples were obtained from the newborn at 32 and 80 hours of life. Mean concentrations of phenoxybenzamine from cord and maternal plasma and in amniotic fluid were 103.3,66, and 79.3 ng/mL, respectively; the newborn's plasma concentration at 32 hours of life was 22.3 ng/mL. At the time of delivery, the 2475-g male infant exhibited perinatal depression; mild transient hypotension was also noted for the first few days of life. DISCUSSION: The fetal—maternal plasma accumulation ratio of 1.6:1 indicates that at this gestational age after 26 days of therapy, the placental transfer of phenoxybenzamine occurs and is accompanied by accumulation in the fetal blood. CONCLUSIONS: Because of the placental transfer of phenoxybenzamine, mild perinatal depression and transient hypotension may occur in newborns of mothers receiving this medication. These newborns must be closely monitored during the first few days of life for respiratory depression and hypotension.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Cuiqin Huang ◽  
Wei Han ◽  
Yajing Fan

Abstract Background We aimed to analyze the correlation between increased fetal movements in the third trimester and neonatal outcomes. Methods We enrolled pregnant women (n = 219) who reported increased/excessive fetal movements in the third trimester in our hospital. A control group of healthy women (n = 278) who had undergone regular childbirth and delivery in our hospital during the same period and did not report abnormal fetal movements were also recruited. All pregnant women underwent fetal non-stress test. We analyzed the neonatal weight, appearance, pulse, grimace, activity, and respiration score, degrees of amniotic fluid contamination, amniotic fluid volume, conditions of umbilical cord around the neck and cord length, and incidence of small for gestational age. In addition, the incidence of preterm delivery, cesarean section rate, postpartum hemorrhage, and other postpartum complications were also analyzed. We then analyzed the correlation between increased/excessive fetal activity and neonatal outcomes. Results Women with complaints of increased/excessive fetal movements exhibited increased fetal movements mainly around 31 and 39 weeks of gestation. Several pregnancy variables, including number of previous delivery, gestational age (less than 34 weeks and more than 37 weeks) and vaginal birth rate, were associated with increased/excessive fetal movements. In addition, women who reported increased/excessive fetal movements had higher odds of large for gestational age (LGA), particularly those with gestational age over 37 weeks. Conclusion Increased/excessive fetal movements may be used to predict adverse neonatal outcome such as LGA.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Camille Fédou ◽  
Benjamin Breuil ◽  
Igor Golovko ◽  
Stéphane Decramer ◽  
Pedro Magalhães ◽  
...  

AbstractProduction of amniotic fluid (AF) is view as predominately driven by excretion of fetal urine (FU). However, the origin of AF peptides, often considered as potential biomarkers of developmental diseases, has never been investigated. Here, we evaluated the FU origin of AF peptides and if the AF peptide content can be used as a surrogate of FU. The abundance of endogenous peptides was analyzed by capillary electrophoresis coupled to mass spectrometry in 216 AF and 64 FU samples. A total of 2668 and 3257 peptides was found in AF and FU respectively. The AF peptidome largely overlapped with the FU peptidome, ranging from 54% in the second pregnancy trimester to 65% in the third trimester. Examination of a subset of 16 paired AF and FU samples revealed that 67 peptides displayed a significant positively correlated abundance in AF and FU, strongly suggesting that their presence in AF was directly associated to FU excretion. As proof-of-concept we showed that measuring the AF abundance of these 67 peptides of FU origin allowed prediction of postnatal renal survival in fetuses with posterior urethral valves. These results demonstrate that the AF peptidome can be considered as a good surrogate of the FU peptidome.


1997 ◽  
Vol 98 (3) ◽  
pp. 767-771 ◽  
Author(s):  
THIERRY PETIT ◽  
MARC DOMMERGUES ◽  
GÉRARD SOCIÉ ◽  
YVES DUMEZ ◽  
ELIANE GLUCKMAN ◽  
...  

1979 ◽  
Vol 95 (3) ◽  
pp. 509-516 ◽  
Author(s):  
B. Obiekwe ◽  
Diana J. Pendlebury ◽  
Y.B. Gordon ◽  
J.G. Grudzinskas ◽  
T. Chard ◽  
...  

1992 ◽  
Vol 134 (2) ◽  
pp. 313-317 ◽  
Author(s):  
M. R. Johnson ◽  
A. Abbas ◽  
K. H. Nicolaides ◽  
S. L. Lightman

ABSTRACT Relaxin was measured in maternal blood and amniotic fluid samples at 9–40 weeks and in fetal blood samples at 19–41 weeks of pregnancy. In amniotic fluid, concentrations of relaxin rose from 58 ng/1 (geometric mean) at 10 weeks to 142 ng/l at 14 weeks and declined subsequently to 55 ng/l at 22 weeks. In maternal blood, mean relaxin concentrations were ten times greater than in amniotic fluid, and concentrations decreased with gestation. Since there was no significant association between the relaxin concentrations in the two compartments, relaxin in the amniotic fluid may be derived from the decidualized endometrium rather than the maternal circulation, alternatively its metabolism may be different in the two compartments. The absence of detectable concentrations of relaxin in any of the fetal blood samples demonstrates that there is no significant placental transfer or fetal synthesis of this peptide. Journal of Endocrinology (1992) 134, 313–317


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