Effect of Ethanol on Prostacyclin, Thromboxane, and Prostaglandin E Production in Human Umbilical Veins

Randall, Carrie L.; Saulnier, Jocelynn L

doi:10.1111/j.1530-0277.1995.tb01576.x

Cited by 19 publications

(12 citation statements)

References 27 publications

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“…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. In summary, alcohol mediated uterine vascular dysfunction does not arise from impairing α1 adrenergic agonist phenylephrine or the prostanoid thromboxane response.…”

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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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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“…Early work in placental biology show that alcohol perfusion in human umbilical veins decreases prostacyclin levels and increases thromboxane/prostacyclin levels [44]. In another study conducted in mice, acute alcohol exposure induced early onset of parturition and was attributed to increased uterine prostaglandin E and F2α levels[45].…”

Section: Discussionmentioning

confidence: 99%

Alcohol-induced alterations in maternal uterine endothelial proteome: A quantitative iTRAQ mass spectrometric approach

Ramadoss¹,

Magness²

2012

Reproductive Toxicology

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Objective To quantitate alcohol-induced alterations in the maternal uterine endothelial proteome utilizing iTRAQ-based mass spectrometry. Study Design Uterine artery endothelial cells from third trimester pregnant ewes were FAC sorted, validated and treated without or with binge-like alcohol. Lysates were trypsin digested, iTRAQ-labeled, and analyzed using nano LC MS/MS. Results Alcohol significantly upregulated 14 and downregulated 17 proteins (P<0.05) including those related to cell structure, transcription/translation regulation, histones, Ca+2/NO, and redox balance. Gene ontology and ArrayTrack analyses revealed alterations to protein processing, binding, and nutrient metabolism pathways. Further, alcohol altered proteins previously correlated with Fetal Alcohol Spectrum Disorders (FASD) and those that regulate epigenetic, transcriptional, and translational processes. Conclusions Alcohol differentially alters the proteome in the maternal uterine compartment at the level of the endothelium. iTRAQ mass spectrometry provides a robust high throughput platform to comprehend the multi-mechanistic actions of alcohol and develop appropriate biomarkers and ameliorative measures for FASD.

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“…The umbilical vein perfusion system was identical to one described previously. 18,37 Briefly, two segments of equal cord length (10 ± 12 cm ) were cut and perfused from placental to fetal direction at a flow rate of 1 ml/min at 37AE C. Portions of the cord that had been clamped or clotted with blood were avoided. Catheters were inserted approximately 1 cm into the vein at both the fetal and the placental end of each segment and sutured in place.…”

Section: Preparation and Perfusion Of Um Bilical Cordsmentioning

confidence: 99%

“…Each segment was placed in its own 37AE C D-PBS bath, connected via catheters to their individual perfusion circuits, and perfused as described previously. 18,37 The two segments were alternately assigned to vehicle and nicotine perfusion conditions in order to control for possible segmental differences in prostaglandin production which have been observed by some investigators. 38 Nicotine exper im ent One segment of each pair of umbilical veins was perfused with Dulbecco's modified Eagle's medium (DM EM ) for the vehicle condition, while the other segment was perfused with nicotine tartrate (Sigma Chemical Co., St Louis, M O, USA ) in vehicle, in a concentration of either 5 mM (n = 7), 10 mM (n = 10) or 20 mM (n = 11).…”

Section: Preparation and Perfusion Of Um Bilical Cordsmentioning

confidence: 99%

“…32 Our laboratory has demonstrated previously that alcohol perfusion of isolated human placental cotyledons increased production of the vasoconstrictive PGE 2 , 19 and perfusion of human umbilical veins with alcohol reduced the vasodilator, prostacyclin, by 50% . 18 Thus, data suggest that alcohol may affect umbilical± placental blood flow through prostaglandins.…”

Section: Introductionmentioning

confidence: 99%

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Physiological concentrations of nicotine do not affect prostacyclin, thromboxane or PGE production from perfused human umbilical veins

et al. 2001

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Smoking dur ing pregna ncy is associated with a num ber of m ater nal and fetal com plications. The m echanism s underlying the effects of nicotine on fetal g rowth and development are not know n, but m ay involve decreases in um bilical± placenta l blood flow. Prostaglandins are vasoactive m ediators that regulate um bilical ± placental blood flow and there is evidence that nicotine m ay alter prostaglandin production. Thus, alterations in vasoactive prostaglandins from the hum an umbilica l vein m ay explain nicotine -induced decreases in vessel blood flow and m ay und erlie some of the negative effects of nicotine on the fetus. This study was designed to deter m ine the relationship between nicotine and hum an um bilica l vein prostaglandin production. Prostacyclin, throm boxane and prostaglandin E were m easured from hum an umbilica l veins collected from wom en at the time of cesarean section. Vessels were perfused with either vehicle (Dulbecco's m odified Eagle' s m edia ), 5 mM, 10 mM or 20 m M nicotine for 60 m inutes. Sam ples were collected from the perfusate after 5, 15, 30 and 60 m inutes of perfusion, and prostaglandins were m easured by radioim munoassay. Data were analyzed by ANOVA. Perfusion with 10 m M or 20 mm significantly reduced prostacyclin production by the hum an um bilical veins, but nicotine did not affect prostaglandin E . The effects of nicotine on throm boxane were less clear. H owever, nicotine concentr ations required to illicit an effect on prostacyclin production were m uch larger than circulating levels associated with smoking , so it is only phar m acological concentr ations that have a significant effect. Thus, nicotine -induced alteration s in um bilical vein prostaglandin production does not appear to be a m echanism by which nicotine adversely affects fetal growth and developm ent.

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Effect of Ethanol on Prostacyclin, Thromboxane, and Prostaglandin E Production in Human Umbilical Veins

Cited by 19 publications

References 27 publications

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

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

Alcohol-induced alterations in maternal uterine endothelial proteome: A quantitative iTRAQ mass spectrometric approach

Physiological concentrations of nicotine do not affect prostacyclin, thromboxane or PGE production from perfused human umbilical veins

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