Greater uterine artery blood flow during pregnancy in multigenerational (Andean) than shorter-term (European) high-altitude residents

Wilson, Megan J.; López, Miriam de la Flor; Vargas, Marco; Julian, Colleen G.; Téllez, Wilma; Rodríguez, Armando; Bigham, Abigail W.; Armaza, J Fernando; Niermeyer, Susan; Shriver, Mark D.; Vargas, Enrique; Moore, Lorna G.

doi:10.1152/ajpregu.00806.2006

Cited by 84 publications

(93 citation statements)

References 44 publications

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“…Hospital-based studies have documented that the risk of adverse perinatal outcomes is increased with extreme maternal Hcts (Moore et al, 2001a;Gonzales et al, 2009) (Fig.4). During pregnancy at high altitude, elevated Hct and the associated increase in blood viscosity contribute to an increased risk of stillbirth, preterm birth, and reduced birth weight, all of which appear to stem from a reduced uterine artery blood flow and, consequently, a reduced rate of O 2 delivery to the uteroplacental circulation (Moore et al, 1982;Moore et al, 2001a;Moore et al, 2001b;Zamudio et al, 1995;Wilson et al, 2007;Julian et al, 2008;Julian et al, 2009b). For this reason, acclimatized lowlanders at high altitude generally experience especially high rates of adverse pregnancy outcomes.…”

Section: Erythropoeitic Activitymentioning

confidence: 99%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

347

343

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SummaryHigh-altitude environments provide ideal testing grounds for investigations of mechanism and process in physiological adaptation. In vertebrates, much of our understanding of the acclimatization response to high-altitude hypoxia derives from studies of animal species that are native to lowland environments. Such studies can indicate whether phenotypic plasticity will generally facilitate or impede adaptation to high altitude. Here, we review general mechanisms of physiological acclimatization and genetic adaptation to high-altitude hypoxia in birds and mammals. We evaluate whether the acclimatization response to environmental hypoxia can be regarded generally as a mechanism of adaptive phenotypic plasticity, or whether it might sometimes represent a misdirected response that acts as a hindrance to genetic adaptation. In cases in which the acclimatization response to hypoxia is maladaptive, selection will favor an attenuation of the induced phenotypic change. This can result in a form of cryptic adaptive evolution in which phenotypic similarity between high-and low-altitude populations is attributable to directional selection on genetically based trait variation that offsets environmentally induced changes. The blunted erythropoietic and pulmonary vasoconstriction responses to hypoxia in Tibetan humans and numerous high-altitude birds and mammals provide possible examples of this phenomenon. When lowland animals colonize high-altitude environments, adaptive phenotypic plasticity can mitigate the costs of selection, thereby enhancing prospects for population establishment and persistence. By contrast, maladaptive plasticity has the opposite effect. Thus, insights into the acclimatization response of lowland animals to high-altitude hypoxia can provide a basis for predicting how altitudinal range limits might shift in response to climate change.

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Section: Erythropoeitic Activitymentioning

confidence: 99%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

347

343

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“…Previously we have shown that uterine artery (UA) diameter and blood flow are lower near term in women residing at high (3,100 m; 10,170 ft, Leadville) compared with low altitude (1,600 m; 5,280 ft, Denver) in Colorado (36). Greater maternal arterial oxygen content and/or UA blood flow, both of which are determinants of uteroplacental oxygen delivery, are associated with protection from SGA at high altitude (20,28,32,35,36). The frequency of preeclampsia, another condition in which UA blood flow is reduced, also increases with altitude and is responsible for approximately one-half of the altitude-associated reduction in birth weight, further demonstrating the importance of adequate UA blood flow to fetal growth at high altitude (13,15).…”

mentioning

confidence: 98%

Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude

Julian

Galan²,

Wilson³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

102

107

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Moore LG. Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude. Am J Physiol Regul Integr Comp Physiol 295: R906 -R915, 2008. First published June 25, 2008 doi:10.1152/ajpregu.00164.2008.-Reduced uteroplacental blood flow is hypothesized to play a key role in altitude-associated fetal growth restriction. It is unknown whether reduced blood flow is a cause or consequence of reduced fetal size. We asked whether determinants of uteroplacental blood flow were altered prior to reduced fetal growth and whether vasoactive and/or angiogenic factors were involved. Women residing at low (LA; 1600 m, n ϭ 18) or high altitude (HA; 3100 m, n ϭ 25) were studied during pregnancy (20, 30, and 36 wk) and 4 mo postpartum (PP) using Doppler ultrasound. In each study, endothelin (ET-1), nitric oxide metabolites (NO x), soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF) levels were quantified. At HA, birth weights were lower (P Ͻ 0.01) and small-for-gestational age was more common (P Ͻ 0.05) compared with LA. HA was associated with lower uterine artery (UA) diameter (P Ͻ 0.01) and blood flow (P Ͻ 0.05). Altitude did not affect ET-1, sFlt-1 or PlGF; however, ET-1/NO x was greater and NOx lower during pregnancy and PP at HA vs. LA. ET-1/NO x was negatively associated with birth weight (20 wk, P Ͻ 0.01; 36 wk, P ϭ 0.05) at LA and HA combined. At HA, UA blood flow (30 wk) was positively associated with birth weight ( †). UA blood flow and ET-1/NO x levels accounted for 45% (20 wk) and 32% (30 wk) of birth weight variation at LA and HA combined, primarily attributed to effects at HA. We concluded that elevated ET-1/NO x and altered determinants of uteroplacental blood flow occur prior to altitude-associated reductions in fetal growth, and therefore, they are likely a cause rather than a consequence of smaller fetal size. fetal growth restriction; hypoxia; small-for-gestational age; uteroplacental oxygen delivery; pregnancy SMALL-FOR-GESTATIONAL AGE (SGA) is a common complication of pregnancy that raises the risk of morbidity and mortality during the perinatal period, as well as in later life (2, 11). Among the many determinants of SGA is the chronic hypoxia of residence at high altitude (Ն2,500 m; 8,200 ft). Birth weight declines progressively, and potently, with increasing altitude such that infants born to women permanently residing at elevations Ն2,500 m are at a greater risk of low birth weight than infants born at lower altitudes (13-15, 34). Altitudinal differences in gestational age, socioeconomic status, parity, maternal height, or the frequency of hypertensive complications do not explain the degree to which birth weight decreases with altitude, indicating that it is likely chronic hypoxia per se that is decreasing fetal growth (12,13,15). Despite the pervasive effect of high altitude on birth weight, the mechanisms by which hypoxia acts to reduce fetal growth are not well understood.A considera...

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“…The weight of the babies born to Tibetan residents at high altitude is more than that of those born to Han women living at the same altitude, which is associated with a higher uterine flow velocity and larger uterine arterial diameters [1]. The uterine arterial diameters in Andean pregnant women are also most doubling increased at high altitude whereas there are about half as much increase in European pregnant women [74]. As a result, Andean pregnant women have much higher uterine blood flows and birth weights of their babies than Europeans at high altitude.…”

Section: Uteroplacental Vascular Systemmentioning

confidence: 99%

Cardiovascular Adaptation to High-Altitude Hypoxia

Ji¹,

Wang²,

Xiao³

2017

Hypoxia and Human Diseases

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High-altitude exposure has been well recognized as a hypoxia exposure that significantly affects cardiovascular function. However, the pathophysiologic adaptation of cardiovascular system to high-altitude hypoxia (HAH) varies remarkably. It may depend on the exposed time and oxygen partial pressure in the altitude place. In short-term HAH, cardiovascular adaptation is mainly characterized by functional alteration, including cardiac functional adjustments, pulmonary vascular constriction, transient pulmonary hypertension, and changes in cerebral blood flow (CBF). These changes may be explained mainly by ventilatory acclimatization and variation of autonomic nervous activity. In long-term HAH, cardiovascular adaptation is mainly characterized by both functional and structural alterations. These changes include right ventricle (RV) hypertrophy, persistent pulmonary hypertension, lower CBF and reduced uteroplacental and fetal volumetric blood flows.

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Greater uterine artery blood flow during pregnancy in multigenerational (Andean) than shorter-term (European) high-altitude residents

Cited by 84 publications

References 44 publications

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Lower uterine artery blood flow and higher endothelin relative to nitric oxide metabolite levels are associated with reductions in birth weight at high altitude

Cardiovascular Adaptation to High-Altitude Hypoxia

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