Disposition of ethanol in maternal blood, fetal blood, and amniotic fluid of third-trimester pregnant ewes

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


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.


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


1969 ◽  
Vol 105 (7) ◽  
pp. 1069-1071 ◽  
Author(s):  
Gerald Carrier ◽  
Arthur S. Hume ◽  
Ben H. Douglas ◽  
Winfred L. Wiser

1996 ◽  
Vol 8 (7) ◽  
pp. 1069 ◽  
Author(s):  
L Gunn ◽  
P Hardiman ◽  
S Tharmaratnam ◽  
D Lowe ◽  
T Chard

The concentrations of interleukin-1 alpha (IL-1 alpha) and IL-6 in pregnancy-associated tissues were investigated in term labour and delivery in the absence of labour (elective Caesarean section). Samples of amniotic fluid, placenta, fetal membranes, umbilical venous and, where possible, umbilical arterial blood were collected at delivery (37-41 weeks of gestation). Maternal blood was sampled during labour. Fluid and tissue extracts were assayed for IL-1 alpha and IL-6 by radioimmunoassay. Placenta and membranes were examined histologically for evidence of infection. Concentrations of IL-1 alpha and IL-6 in amniotic fluid and membrane extract, and IL-1 alpha in maternal and fetal blood, were raised after the onset of labour. Concentrations of both cytokines in the placenta remained unchanged. There was a good correlation between concentrations of both cytokines in amniotic fluid and membranes. There was also a significant correlation between concentrations of IL-1 alpha and IL-6 in amniotic fluid, placenta and membranes. It is suggested that the fetal membranes or maternal decidua, but not the placenta, internal fetal or maternal tissues, are the main sources of IL-1 alpha and IL-6 during labour.


1991 ◽  
Vol 47 (2) ◽  
pp. 184-189 ◽  
Author(s):  
Masatoshi Hayashi ◽  
Yasuie Shimazaki ◽  
Shinichi Kamata ◽  
Norihide Kakiichi ◽  
Masashi Ikeda

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