Effect of ethanol on thromboxane and prostacyclin production in the human placenta

Siler-Khodr, Theresa M.; Yang, Yuxiao; Grayson, Marcia H.; Henderson, George I.; Lee, Makau; Schenker, Steven

doi:10.1016/s0741-8329(00)00084-7

Cited by 23 publications

(17 citation statements)

References 37 publications

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“…In contrast, an earlier study conducted in drinking pregnant women who consumed higher amounts of alcohol (5-to 20-yr history of alcohol abuse; consumption, ϳ140 -840 g/wk during first half of gestation or beyond) showed the ratio of the urinary combined prostacyclin metabolites (vasodilator) and thromboxane B 2 (vasoconstrictor) to be significantly lower compared with that in the controls (101). Similar observations were found in the fetoplacental compartment; alcohol perfusion (240 min or 60 min; 200 or 300 mg%) of single human cotyledons increased the ratio of thromboxane to prostacyclin at few time points (80). Randall and Saulnier (72) have demonstrated that perfusion (100 mM) in human umbilical veins showed an increased thromboxane-to-prostacyclin ratio at all time points.…”

Section: Effects Of Alcohol On Maternal Endocrine and Paracrine Systesupporting

confidence: 66%

Vascular effects of maternal alcohol consumption

Ramadoss

Magness

2012

American Journal of Physiology-Heart and Circulatory Physiology

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Maternal alcohol consumption during pregnancy is a significant field of scientific exploration primarily because of its negative effects on the developing fetus, which is specifically defined as fetal alcohol spectrum disorders. Though the effects on the mother are less explored compared with those on the fetus, alcohol produces multiple effects on the maternal vascular system. Alcohol has major effects on systemic hemodynamic variables, endocrine axes, and paracrine factors regulating vascular resistance, as well as vascular reactivity. Alcohol is also reported to have significant effects on the reproductive vasculature including alterations in blood flow, vessel remodeling, and angiogenesis. Data presented in this review will illustrate the importance of the maternal vasculature in the pathogenesis of fetal alcohol spectrum disorders and that more studies are warranted in this field.

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Section: Effects Of Alcohol On Maternal Endocrine and Paracrine Systesupporting

confidence: 66%

Vascular effects of maternal alcohol consumption

Ramadoss

Magness

2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…In contrast, the offspring (25 weeks of age) of mothers administered alcohol (ethanol-containing diet had 36% of total calories) during pregnancy exhibited significant attenuation of norepinephrine vasoconstrictive response in the aortic rings (Turcotte et al, 2002). Although no one has reported alcohol effects on thromboxane vasoconstrictive response during pregnancy to our knowledge, alcohol perfusion (240 min or 60 min; 200 or 300 mg%) of human cotyledons increased the ratio of thromboxane (vasoconstrictor) to prostacyclin (vasodilator) at a few time points (Siler-Khodr et al, 2000). Randall and colleagues (Randall and Saulnier, 1995) have demonstrated that alcohol perfusion (100 mM) in human umbilical veins showed an increased thromboxane-to-prostacyclin ratio at all time points.…”

Section: Discussionmentioning

confidence: 99%

Chronic Binge Alcohol Exposure During Pregnancy Impairs Rat Maternal Uterine Vascular Function

Subramanian

Naik

Sathishkumar

et al. 2014

Alcohol Clin Exp Res

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Background Alcohol exposure during pregnancy results in an array of structural and functional abnormalities called Fetal Alcohol Spectrum Disorders (FASD). Alcohol dysregulates the exquisite coordination and regulation of gestational adaptations at the level of the uterine vasculature. We herein hypothesized that chronic binge-like alcohol impairs maternal uterine artery reactivity to vasoconstrictors and dilators and that alcohol-induced vascular dysfunction is dependent on the endothelium. Methods We utilized a once-daily binge alcohol (4.5 g/kg body weight) exposure paradigm (gestational day (GD) 7-17) in a pregnant rat model system and investigated primary uterine artery function in response to vasoconstrictors and vasodilators utilizing wire myography. Results Alcohol (peak blood alcohol concentration, 216 mg/dl) produced uterine vascular dysfunction in the absence of grossly observable growth deficits in maternal and fetal body weights, fetal crown-rump length and placental weight. Alcohol did not produce altered uterine vascular reactivity to α1 adrenergic agonist phenylephrine or the prostanoid thromboxane. However, alcohol specifically impaired endothelium-dependent acetylcholine (Ach)-mediated uterine artery vasodilation but exogenous endothelium-independent vasodilators like sodium nitroprusside exhibited no alcohol effect; Ach significantly decreased vessel relaxation (P=0.003; ↓pD2 (negative log molar Ach concentration producing the half maximum response), −7.004±0.215 vs. −6.310±0.208; EMax (maximal Ach response), 92% vs. 75%). Conclusion We conclude that moderate alcohol exposure impairs uterine vascular function in pregnant mothers. Alcohol specifically impairs endothelium-dependent agonist-induced uterine artery vasodilation. In summary, the maternal uterine compartment may play a significant role in the pathogenesis of FASD. Thus, the mechanistic targets of alcohol at the level of both the mother and the fetus need to be considered in order to develop effective therapeutic treatment strategies for FASD.

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“…Alcohol is most teratogenic during organogenesis (gestational week 9 to 11) and may destroy placental trophoblastic cells, increase thromboxane production and reduce the utero-placental blood flow [90,91]. Moderate alcohol consumption (less than 14 drinks a week) does not seem to increase the risk of IUGR [92].…”

Section: Alcohol Consumptionmentioning

confidence: 99%

Growth Restriction: Etiology, Maternal and Neonatal Outcome. A Review

Haram¹,

Svendsen²,

Myking

2007

CWHR

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Intrauterine growth restriction (IUGR) is an important clinical problem associated with increased perinatal mortality and morbidity. The most preferred small for gestational age (SGA) definition is birth weight below the 10th percentile, adjusted for gestational age. The incidence of IUGR is about 4 to 7 %. A variety of hormones are involved. IUGR may be due to chromosomal defects, smoking, early-onset preeclampsia (< 34 weeks), connective tissue and inflammatory rheumatic diseases, maternal infections, several drugs, twin-to twin transfusion, anorexia nervosa, low maternal pre-pregnancy or small weight gain during pregnancy. High hemoglobin (Hb) levels during the first 10-20 weeks of pregnancy may also cause IUGR. Complications due to IUGR include fetal or neonatal death, dysmaturity, and physical as well as temporary or permanent mental defects. Low birth weight children may have behavioral problems, psychiatric disorders and lower intelligence test scores later in life. There is a relationship between IUGR, timing and progression of puberty, and polycystic ovary syndrome. Fetal changes of lipid metabolism and homeostasis in IUGR may place the grown adult at risk for hypertension, diabetes mellitus and coronary artery disease. Mothers of low weight offspring have an increased risk for cardiovascular and kidney disease later in life.

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Effect of ethanol on thromboxane and prostacyclin production in the human placenta

Cited by 23 publications

References 37 publications

Vascular effects of maternal alcohol consumption

Vascular effects of maternal alcohol consumption

Chronic Binge Alcohol Exposure During Pregnancy Impairs Rat Maternal Uterine Vascular Function

Growth Restriction: Etiology, Maternal and Neonatal Outcome. A Review

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