Effects of chronic hypoxia on cardiac function measured by pressure-volume catheter in fetal chickens

Jonker, Sonnet S.; Giraud, G; Espinoza, Herbert M.; Davis, Erica; Crossley, Dane A.

doi:10.1152/ajpregu.00484.2014

Cited by 24 publications

(19 citation statements)

References 58 publications

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“…Although changes in heart morphology that would indicate changes in heart performance didnot occur, this does not mean that stroke volume and cardiac output do not actually change. Certainly, cardiovascular responses to hypoxia have been well documented in the middle to late embryos of galliform and ratite birds [ 36 – 38 ] [ 71 – 74 ] and may have occurred in the present study on quail embryos.…”

Section: Discussionmentioning

confidence: 62%

Critical developmental windows for morphology and hematology revealed by intermittent and continuous hypoxic incubation in embryos of quail (Coturnix coturnix)

Burggren

Elmonoufy

2017

PLoS ONE

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Hypoxia during embryonic growth in embryos is frequently a powerful determinant of development, but at least in avian embryos the effects appear to show considerable intra- and inter-specific variation. We hypothesized that some of this variation may arise from different protocols that may or may not result in exposure during the embryo’s critical window for hypoxic effects. To test this hypothesis, quail embryos (Coturnix coturnix) in the intact egg were exposed to hypoxia (~15% O2) during “early” (Day 0 through Day 5, abbreviated as D0-D5), “middle” (D6-D10) or “late” (D11-D15) incubation or for their entire 16–18 day incubation (“continuous hypoxia”) to determine critical windows for viability and growth. Viability, body mass, beak and toe length, heart mass, and hematology (hematocrit and hemoglobin concentration) were measured on D5, D10, D15 and at hatching typically between D16 and D18 Viability rate was ~50–70% immediately following the exposure period in the early, middle and late hypoxic groups, but viability improved in the early and late groups once normoxia was restored. Middle hypoxia groups showed continuing low viability, suggesting a critical period from D6-D10 for embryo viability. The continuous hypoxia group experienced viability reaching <10% after D15. Hypoxia, especially during late and continuous hypoxia, also inhibited growth of body, beak and toe when measured at D15. Full recovery to normal body mass upon hatching occurred in all other groups except for continuous hypoxia. Contrary to previous avian studies, heart mass, hematocrit and hemoglobin concentration were not altered by any hypoxic incubation pattern. Although hypoxia can inhibit embryo viability and organ growth during most incubation periods, the greatest effects result from continuous or middle incubation hypoxic exposure. Hypoxic inhibition of growth can subsequently be “repaired” by catch-up growth if a final period of normoxic development is available. Collectively, these data indicate a critical developmental window for hypoxia susceptibility during the mid-embryonic period of development.

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Section: Discussionmentioning

confidence: 62%

Critical developmental windows for morphology and hematology revealed by intermittent and continuous hypoxic incubation in embryos of quail (Coturnix coturnix)

Burggren

Elmonoufy

2017

PLoS ONE

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“…Growth restriction and increased relative organ mass are common morphological signatures in a range of vertebrates subjected to developmental hypoxia [mammals (58, 60); birds (16, 27, 43, 50); reptiles (12, 18, 69)]. The relative increase in heart mass may be due to a suppression of somatic growth, a response of the cardiac tissue to hypoxia directly, or to a secondary response due to endocrine or hemodynamic changes in the embryonic system.…”

Section: Discussionmentioning

confidence: 99%

Developmental plasticity of mitochondrial function in American alligators,Alligator mississippiensis

Galli

Crossley

Elsey

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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The effect of hypoxia on cellular metabolism is well documented in adult vertebrates, but information is entirely lacking for embryonic organisms. The effect of hypoxia on embryonic physiology is particularly interesting, as metabolic responses during development may have life-long consequences, due to developmental plasticity. To this end, we investigated the effects of chronic developmental hypoxia on cardiac mitochondrial function in embryonic and juvenile American alligators (Alligator mississippiensis). Alligator eggs were incubated in 21% or 10% oxygen from 20 to 90% of embryonic development. Embryos were either harvested at 90% development or allowed to hatch and then reared in 21% oxygen for 3 yr. Ventricular mitochondria were isolated from embryonic/juvenile alligator hearts. Mitochondrial respiration and enzymatic activities of electron transport chain complexes were measured with a microrespirometer and spectrophotometer, respectively. Developmental hypoxia induced growth restriction and increased relative heart mass, and this phenotype persisted into juvenile life. Embryonic mitochondrial function was not affected by developmental hypoxia, but at the juvenile life stage, animals from hypoxic incubations had lower levels of Leak respiration and higher respiratory control ratios, which is indicative of enhanced mitochondrial efficiency. Our results suggest developmental hypoxia can have life-long consequences for alligator morphology and metabolic function. Further investigations are necessary to reveal the adaptive significance of the enhanced mitochondrial efficiency in the hypoxic phenotype.

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“…Collectively, studies in the chicken embryo suggest that cardiovascular dysfunction in children and in mammalian animal models of IUGR pregnancy may again be attributable to chronic fetal hypoxia. Thus, incubation of chicken embryos under hypoxic conditions was also associated with reduced left ventricular ejection fraction and contractility, and diminished left ventricular developed pressure, all indicative of significant systolic dysfunction (Rouwet et al 2002;Sharma et al 2006;Tintu et al 2009;Jonker et al 2015;Itani et al 2016). Several candidate pathways may contribute to the hypoxia-induced cardiovascular dysfunction, including those involving vascular endothelial growth factor (VEGF) (Tintu et al 2009;Moonen et al 2012;Itani et al 2016) and Rho-kinase (Zoer et al 2010).…”

Section: Chronic Fetal Hypoxia and Programmed Cardiovascular Risk: Stmentioning

confidence: 99%

The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo

Itani

Salinas

Villena

et al. 2017

The Journal of Physiology

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It is now established that adverse conditions during pregnancy can trigger a fetal origin of cardiovascular dysfunction and/or increase the risk of heart disease in later life. Suboptimal environmental conditions during early life that may promote the development of cardiovascular dysfunction in the offspring include alterations in fetal oxygenation and nutrition as well as fetal exposure to stress hormones, such as glucocorticoids. There has been growing interest in identifying the partial contributions of each of these stressors to programming of cardiovascular dysfunction. However, in humans and in many animal models this is difficult, as the challenges cannot be disentangled. By using the chicken embryo as an animal model, science has been able to circumvent a number of problems. In contrast to mammals, in the chicken embryo the effects on the developing cardiovascular system of changes in oxygenation, nutrition or stress hormones can be isolated and determined directly, independent of changes in the maternal or placental physiology. In this review, we summarise studies that have exploited the chicken embryo model to determine the effects on prenatal growth, cardiovascular development and pituitary-adrenal function of isolated chronic developmental hypoxia.

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Effects of chronic hypoxia on cardiac function measured by pressure-volume catheter in fetal chickens

Cited by 24 publications

References 58 publications

Critical developmental windows for morphology and hematology revealed by intermittent and continuous hypoxic incubation in embryos of quail (Coturnix coturnix)

Critical developmental windows for morphology and hematology revealed by intermittent and continuous hypoxic incubation in embryos of quail (Coturnix coturnix)

Developmental plasticity of mitochondrial function in American alligators,Alligator mississippiensis

The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo

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