Vascular function in alcohol-treated pregnant and nonpregnant mice

2001 ◽  
Vol 281 (5) ◽  
pp. R1449-R1455 ◽  
Author(s):  
Jocelynn L. Cook ◽  
Yunlong Zhang ◽  
Sandra T. Davidge
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Vascular System ◽  
Prenatal Alcohol Exposure ◽  
Control Diet ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Vascular Response ◽  
Oxide Component ◽  
Pregnant Mice

The effect of alcohol on maternal vascular adaptations to pregnancy is unknown. This study was designed to determine the effect of alcohol consumption on nitric oxide-mediated vascular function in mice during pregnancy. Female pregnant or nonpregnant C57BL/6J mice were fed a control diet or a liquid diet of 25% ethanol-derived calories for 13 days (from gestational days 6–18). Phenylephrine vasoconstriction was blunted in pregnancy compared with the nonpregnant state due to enhanced nitric oxide modulation, which was impaired by ethanol exposure. Although the EC50 and maximal responses to methacholine were not different in nonpregnant vs. pregnant mice, the nitric oxide component to methacholine-induced vasorelaxation was greater in the pregnant mice. Interestingly, alcohol affected only the pregnant animals in their response to methacholine. These data indicate that alcohol reduced the nitric oxide modulation of vascular response, which was more pronounced during pregnancy. These studies provide novel information regarding the effects of alcohol on the maternal vascular system during pregnancy and thereby contribute to further understanding of the adverse effects associated with prenatal alcohol exposure.

Forearm Vascular Response to Nitric Oxide and Calcitonin Gene- Related Peptide: Comparison between Migraine Patients and Control Subjects

Cephalalgia ◽  
2006 ◽  
Vol 26 (1) ◽  
pp. 56-63 ◽  
Author(s):  
JNJM de Hoon ◽  
P Smits ◽  
J Troost ◽  
HAJ Struijker-Boudier ◽  
LMAB Van Bortel
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Venous Occlusion ◽  
Calcitonin Gene Related Peptide ◽  
Vascular Response ◽  
No Donor ◽  
Related Peptide ◽  
Control Subjects ◽  
Calcitonin Gene ◽  
Endogenous Release

The forearm vascular response to nitric oxide (NO) and calcitonin gene-related peptide (CGRP) was investigated in 10 migraine patients and 10 matched control subjects. Changes in forearm blood flow (FBF) during intrabrachial infusion of: (i) serotonin (releasing endogenous NO), (ii) sodium nitroprusside (SNP, exogenous NO-donor), and (iii) CGRP were measured using venous occlusion plethysmography. Flow-mediated dilation (FMD) of the brachial artery, a measure for the endogenous release of NO reactive to occlusion, was measured using ultrasound and expressed as percentage change vs. baseline diameter. FBF ratio (i.e. FBF in the infused over the control arm) at baseline (1.1 ± 0.1) did not differ between both populations. Serotonin, SNP and CGRP induced a dose-dependent increase ( P < 0.001) in FBF ratio in controls (to 2.8 ± 0.3, 6.7 ± 1.4 and 6.9 ± 1.2 at the highest dose, respectively) and migraineurs (2.5 ± 0.4, 5.6 ± 0.8 and 6.5 ± 1.3, respectively); these ratios did not differ between both groups. FMD was comparable in control subjects (5.8 ± 1%) and migraine patients (5.2 ± 1%). Based on the forearm vascular response to NO and CGRP, migraine patients do not display generalized changes in vascular function.

scholarly journals Prenatal exposure to alcohol alters the Golgi apparatus of newborn rat hepatocytes: a cytochemical study.

1987 ◽  
Vol 35 (2) ◽  
pp. 221-228 ◽  
Author(s):  
J Renau-Piqueras ◽  
F Miragall ◽  
C Guerri ◽  
R Baguena-Cervellera
Keyword(s):  
Golgi Apparatus ◽  
Prenatal Exposure ◽  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Rat Hepatocytes ◽  
Ethanol Exposure ◽  
Newborn Rat ◽  
Cytochemical Study ◽  
Cerium Phosphate ◽  
Osmium Impregnation

The effect of prenatal exposure to ethanol on the Golgi apparatus of newborn rat hepatocytes has been studied cytochemically using several trans-Golgi markers (thiamine pyrophosphatase, uridine diphosphatase, inosine diphosphatase, acid phosphatase, and 5'-nucleotidase) as well as a cis-side marker (osmium impregnation). The amount of cerium phosphate formed in the cytochemical reactions was roughly quantitated by stereologic methods. The Golgi apparatus of about 40% of the hepatocytes appeared disorganized after alcohol treatment, and in the other 60%, the electron density of reaction product deposits for all phosphatases investigated was decreased. 5'-Nucleotidase was completely absent in cisternae of Golgi apparatus of treated cells. In control cells impregnated with osmium tetroxide, reduced osmium compounds were observed in most Golgi cisternae and in nearby vesicles. In contrast, only small vesicles appeared positive in treated hepatocytes. These results suggest that prenatal alcohol exposure alters some Golgi functions. Thus, the decrease in nucleoside diphosphatase and 5'-nucleotidase cytochemical activities after ethanol exposure strongly suggests that this treatment could affect glycosylation in the Golgi apparatus of newborn rat hepatocytes.

scholarly journals Maternal circulating miRNAs that predict infant FASD outcomes influence placental maturation

2019 ◽  
Vol 2 (2) ◽  
pp. e201800252 ◽  
Author(s):  
Alexander M Tseng ◽  
Amanda H Mahnke ◽  
Alan B Wells ◽  
Nihal A Salem ◽  
Andrea M Allan ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Epithelial Mesenchymal Transition ◽  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Growth Restriction ◽  
Circulating Mirnas ◽  
Placental Development ◽  
Mesenchymal Transition ◽  
Pregnant Mice

Prenatal alcohol exposure (PAE), like other pregnancy complications, can result in placental insufficiency and fetal growth restriction, although the linking causal mechanisms are unclear. We previously identified 11 gestationally elevated maternal circulating miRNAs (HEamiRNAs) that predicted infant growth deficits following PAE. Here, we investigated whether theseHEamiRNAs contribute to the pathology of PAE, by inhibiting trophoblast epithelial–mesenchymal transition (EMT), a pathway critical for placental development. We now report for the first time that PAE inhibits expression of placental pro-EMT pathway members in both rodents and primates, and thatHEamiRNAs collectively, but not individually, mediate placental EMT inhibition.HEamiRNAs collectively, but not individually, also inhibited cell proliferation and the EMT pathway in cultured trophoblasts, while inducing cell stress, and following trophoblast syncytialization, aberrant endocrine maturation. Moreover, a single intravascular administration of the pooled murine-expressedHEamiRNAs, to pregnant mice, decreased placental and fetal growth and inhibited the expression of pro-EMT transcripts in the placenta. Our data suggest thatHEamiRNAs collectively interfere with placental development, contributing to the pathology of PAE, and perhaps also, to other causes of fetal growth restriction.

Folic acid prevents functional and structural heart defects induced by prenatal ethanol exposure

2021 ◽  
Author(s):  
Stephanie M Ford ◽  
Cameron J Pedersen ◽  
Matthew R Ford ◽  
Jun W Kim ◽  
Ganga H Karunamuni ◽  
...  
Keyword(s):  
Blood Flow ◽  
Folic Acid ◽  
Heart Diseases ◽  
Prenatal Alcohol Exposure ◽  
Heart Defects ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Endocardial Cushion ◽  
Prenatal Ethanol Exposure ◽  
Endocardial Cushions

Increased regurgitant blood flow has been linked to endocardial cushion defects and resultant congenital heart diseases (CHDs). Prenatal alcohol exposure (PAE) has been shown to alter early blood flow resulting in abnormal endocardial cushions and CHDs. Compounds, including folic acid (FA), mitigate PAE effects and prevent CHDs, but few studies have assessed their effects on blood flow. We modeled binge drinking in quail embryos at gastrulation. Embryos were exposed to ethanol alone, FA (3.2 μg/egg) alone, and the two simultaneously. We quantified in cardiac looping stages (equivalent to 4 weeks of human gestation) regurgitant blood flow with Doppler optical coherence tomography (OCT) and endocardial cushion volumes using OCT imaging. Incidences of abnormal body curvature and heart rates were also measured. Embryos exposed to ethanol showed significantly increased regurgitant blood flow compared to controls, while embryos given FA with ethanol had significantly reduced regurgitant blood flow but did not return to control levels. Ethanol exposure led to significantly smaller, abnormal endocardial cushions and the addition of FA improved their size, but they remained smaller than controls. Abnormal body curvatures after PAE were reduced in incidence but not fully prevented by FA. FA supplementation partially alleviated PAE induced abnormal cardiovascular function and morphology. Normal blood flow and endocardial cushions are both required to produce a healthy four-chambered heart. These findings support that FA supplementation should begin early in pregnancy to prevent heart as well as neural tube defects. Investigations into the efficacy of combinations of compounds to prevent PAE-induced defects is warranted.

scholarly journals Vascular senescence and ageing: a role for the MEOX proteins in promoting endothelial dysfunction

2017 ◽  
Vol 95 (10) ◽  
pp. 1067-1077 ◽  
Author(s):  
Josette M. Northcott ◽  
Michael P. Czubryt ◽  
Jeffrey T. Wigle
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Vascular Function ◽  
Vascular System ◽  
Vascular Dysfunction ◽  
Enos Expression ◽  
Angiogenic Potential ◽  
Protein Levels ◽  
Increased Risk

In the vascular system, ageing is accompanied by the accrual of senescent cells and is associated with an increased risk of vascular disease. Endothelial cell (EC) dysfunction is a hallmark of vascular disease and is characterized by decreased angiogenic potential, reduced nitric oxide bioavailability, impaired vasodilation, increased production of ROS, and enhanced inflammation. In ECs, the major producer of nitric oxide is the endothelial nitric oxide synthase (eNOS) enzyme that is encoded by the NOS3 gene. NOS3/eNOS function is tightly regulated at both the transcriptional and post-transcriptional levels to maintain normal vascular function. A key transcriptional regulator of eNOS expression is p53, which has been shown to play a central role in mediating cellular senescence and thereby vascular dysfunction. Herein, we show that, in ECs, the MEOX homeodomain transcription factors decrease the expression of genes involved in angiogenesis, repress eNOS expression at the mRNA and protein levels, and increase the expression of p53. These findings support a role for the MEOX proteins in promoting endothelial dysfunction.

scholarly journals NGF and BDNF Alterations by Prenatal Alcohol Exposure

2019 ◽  
Vol 17 (4) ◽  
pp. 308-317 ◽  
Author(s):  
Valentina Carito ◽  
Mauro Ceccanti ◽  
Giampiero Ferraguti ◽  
Roberto Coccurello ◽  
Stefania Ciafrè ◽  
...  
Keyword(s):  
Prenatal Alcohol Exposure ◽  
Neuronal Cell Death ◽  
Antioxidant Properties ◽  
Neuronal Cell ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Signalling Pathways ◽  
Prenatal Ethanol Exposure ◽  
Developmental Defects ◽  
Prenatal Alcohol

Background: It is now widely established that the devastating effects of prenatal alcohol exposure on the embryo and fetus development cause marked cognitive and neurobiological deficits in the newborns. The negative effects of the gestational alcohol use have been well documented and known for some time. However, also the subtle role of alcohol consumption by fathers prior to mating is drawing special attention. Objective: Both paternal and maternal alcohol exposure has been shown to affect the neurotrophins' signalling pathways in the brain and in target organs of ethanol intoxication. Neurotrophins, in particular nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are molecules playing a pivotal role in the survival, development and function of the peripheral and central nervous systems but also in the pathogenesis of developmental defects caused by alcohol exposure. Methods: New researches from the available literature and experimental data from our laboratory are presented in this review to offer the most recent findings regarding the effects of maternal and paternal prenatal ethanol exposure especially on the neurotrophins' signalling pathways. Results: NGF and BDNF changes play a subtle role in short- and long-lasting effects of alcohol in ethanol target tissues, including neuronal cell death and severe cognitive and physiological deficits in the newborns. Conclusion: The review suggests a possible therapeutic intervention based on the use of specific molecules with antioxidant properties in order to induce

Complex Trauma and Prenatal Alcohol Exposure: Clinical Implications

2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Child Development ◽  
Academic Outcomes ◽  
Complex Trauma ◽  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Clinical Implications ◽  
Prenatal Alcohol ◽  
The Brain

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.

Sign in / Sign up

Export Citation Format

Share Document