The placenta and the newborn infant at high altitudes

Krüger, H; Arias‐Stella, Javier

doi:10.1016/0002-9378(70)90045-1

Cited by 129 publications

(55 citation statements)

References 11 publications

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“…Importantly, the level of FGR, placental weight, and mean placenta-to-fetus ratio achieved in our studies was similar to that achieved by others (11,22,24). Furthermore, we did not observe an increase in fetal mortality, which might have introduced an additional variable.…”

Section: Discussionsupporting

confidence: 90%

Magnetic resonance imaging of hypoxic injury to the murine placenta

Tomlinson

Garbow

Anderson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionsupporting

confidence: 90%

Magnetic resonance imaging of hypoxic injury to the murine placenta

Tomlinson

Garbow

Anderson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Oestrogen administration improves arterial endothelium-dependent vasodilation 27 and in postmenopausal women in vivo, oestrogens enhance NO derivatives and improve endothelium-dependent vasodilation 28 -32 . In pregnancy at high altitude, maternal venous oestrogen levels and urinary oestrogen secretion have been shown to be lower than those of mothers at sea level 33,34 . However, oestrogen upregulation of NO production appears to reach a plateau, above which increase in oestrogen levels does not increase further NO production 28,29 .…”

Section: Discussionmentioning

confidence: 96%

Flow-mediated dilatation of the brachial artery in pregnancy at high altitude

Kametas¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective Pregnancy at high altitude has been associated with increased prevalence of pre-eclampsia and reduced maternal oestrogen levels, factors that have been associated with endothelial dysfunction. The aim of this study was to examine the effect of high altitude (4370 m above sea level) on endothelial function during pregnancy as assessed by a non-invasive method. Design Cross-sectional study.Setting Two maternity units providing routine antenatal care: one at high altitude (District General Hospital -IPSS in Cerro de Pasco, Peru) and one at sea level (Instituto Materno-Perinatal in Lima, Peru). Population Sixty pregnant women at 6 -42 weeks of gestation resident at high altitude (Cerro de Pasco, Peru, 4370 m above sea level) and 54 at sea level (Lima, Peru). Comparisons were performed also in 11 and 14 non-pregnant women at each altitude, respectively. Methods Endothelial function was assessed by flow-mediated dilatation of the brachial artery using highresolution ultrasound. Main outcome measures Differences in flow mediated dilatation of the brachial artery in two groups of pregnant women, one at high altitude and one at sea level. Results Both at high altitude and sea level flow-mediated dilatation of the brachial artery increased in the first two trimesters to levels 32% higher than non-pregnant controls. However, in the third trimester, flowmediated dilatation of the brachial artery was lower than non-pregnant levels. Resting vessel size increased during pregnancy by 15% compared with non-pregnant controls at term, with no difference between the two populations at high and low altitude. Pregnancy at high altitude, compared with sea level, was associated with 59% lower baseline blood flow and 76% higher reactive hyperaemia. Similarly, non-pregnant controls at high altitude compared with sea level demonstrated similar flow-mediated dilatation of the brachial artery and 40% lower resting blood flow of the brachial artery. However, the difference in reactive hyperaemia did not reach statistical significance. Conclusion These data suggest that, during pregnancy at high altitude, endothelial function, as assessed by flow-mediated dilatation of the brachial artery, is not impaired.

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“…Indeed, reductions in placental efficiency are linked to compensatory increases in placental growth and hypertrophy (7,112). Higgins et al (67) found that obesity is associated with placental hypertrophy along with reduced cell turnover, which are both characteristics of a fetal hypoxic insult (37,85). These findings suggest that obesity-related metabolic factors may attenuate cytotrophoblast-mediated spiral artery remodeling thereby contributing to the development of placental ischemia-induced hypertension.…”

Section: Effects Of Obesity On the Placental Function And Perfusionmentioning

confidence: 99%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

114

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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The placenta and the newborn infant at high altitudes

Cited by 129 publications

References 11 publications

Magnetic resonance imaging of hypoxic injury to the murine placenta

Magnetic resonance imaging of hypoxic injury to the murine placenta

Flow-mediated dilatation of the brachial artery in pregnancy at high altitude

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

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