Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution

Kamitomo, Masato; Alonso, Justo; Okai, Takashi; Longo, Lawrence D.; Gilbert, R. D.

doi:10.1016/0002-9378(93)90646-z

Cited by 99 publications

(87 citation statements)

References 9 publications

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“…By contrast, the latter mechanism can promote a redistribution of blood flow away from peripheral tissues during hypoxia in favor of hypoxiasensitive tissues, such as the heart and brain (Hochachka, 1985). This reduction in blood flow to peripheral tissues might help animals tolerate short periods of O 2 lack, but it is not overcome after prolonged acclimatization to high altitude (Kamitomo et al, 1993;Hansen and Sander, 2003). Peripheral O 2 supply can remain impaired even when pulmonary and hematological adjustments restore arterial oxygenation to normoxic levels (Calbet et al, 2003), possibly because of the complex integration of feedforward and feedback influences from the central nervous system, the heart and the peripheral tissues (Noakes et al, 2004).…”

Section: Tissue O 2 Transportmentioning

confidence: 99%

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

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

338

329

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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: Tissue O 2 Transportmentioning

confidence: 99%

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

Storz

Scott

Cheviron

2010

Journal of Experimental Biology

338

329

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“…Sudden infant death has also been associated with low oxygenation (Southall and Samuels 1989). As a result of low oxygenation, extensive redistribution of blood takes place in the brain and heart (Kamitomo et al 1993). In particular, left ventricular functions are significantly depressed under such conditions.…”

Section: Introductionmentioning

confidence: 99%

Effects of hypoxia on stress proteins in the piglet heart at birth

Louapre

Grongnet²,

Tanguay

et al. 2005

Cell Stress Chaper

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Hypoxia at birth represents a very stressful event that can result in severe lifelong consequences in different tissues, including those of the heart. Heat shock and other associated stress proteins are involved in cellular protection, but their roles are not clearly defined at the time of birth. Newborn piglets were subjected to 5% oxygen and 95% nitrogen for either 1 or 4 hours. They were allowed to recover over periods of 1 to 68 hours. The relative levels of ␣B-crystallin, HspB8, Hsp20, Hsp27, Hsp60, and Hsp70 as well as nitric oxide synthases (NOS) (endothelial NOS, inducible NOS, neuronal NOS) were examined by Western blot analysis. Surprisingly, ␣B-crystallin expression was drastically increased in animals submitted to hypoxia. The hypoxia-associated factor HIFI␣ was also strongly and rapidly overexpressed. Heme oxygenase 1 was also increased. To a lesser extent, neuronal NOS was also increased in the left ventricle of animals submitted to hypoxia. This work clearly shows that the Hsp chaperone ␣B-crystallin is strongly overexpressed in the left ventricle of animals submitted to hypoxia. This observation dissociates the response to low oxygenation of ␣B-crystallin and other stress-associated proteins including Hsp27, and it indicates that heme oxygenase is not alone among HSPs in its oxygen-related gene expression.

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“…Furthermore, 9 days of umbilical placental embolization resulted in reduced placental blood flow and decreases in fetal weight and fetal hypoxemia, but it did not result in redistribution of blood flow to the major organs (5). Long-term hypoxia in pregnant ewes living at high altitude resulted in fetuses with lower right and combined ventricular output (40), but no change in blood flow to the brain or heart (39); however, the fetuses were not growth-restricted and had the same oxygen content as controls (40). There have been no studies, however, that have investigated the impact of placental insufficiency and chronic fetal hypoxemia coupled with fetal growth restriction on regional blood flow in the fetus in late gestation.…”

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confidence: 99%

Impact of chronic hypoxemia on blood flow to the brain, heart, and adrenal gland in the late-gestation IUGR sheep fetus

Paudel

McMillen

Dunn

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

100

102

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Effects of long-term, high-altitude hypoxemia on ovine fetal cardiac output and blood flow distribution

Cited by 99 publications

References 9 publications

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

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

Effects of hypoxia on stress proteins in the piglet heart at birth

Impact of chronic hypoxemia on blood flow to the brain, heart, and adrenal gland in the late-gestation IUGR sheep fetus

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