In vitro study of rat embryos. I. Effects of decreased oxygen on embryonic heart rate

Shepard, Thomas H.; Tanimura, Takashi; Robkin, Maurice A.

doi:10.1002/tera.1420020205

Cited by 26 publications

(5 citation statements)

References 4 publications

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“…Further support for our hypothesis is the observation that oxygen is toxic to day 10 rat embryos, a finding known for some time (Shepard et al, 1969;New and Coppola, 1970) and it is standard practice at this early stage to culture explanted rat and mouse embryos in 10% or less oxygen (New, 1973). Furthermore, exposure to carbon monoxide which inhibits the terminal electron transport system has no adverse effects on the day 10 embryo (Robkin, 1997).…”

Section: Discussionmentioning

confidence: 54%

Ultrastructural study of mitochondria and their cristae in embryonic rats and primate (N. nemistrina)

1998

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Information on the morphology of mitochondria during embryogenesis is scattered in the literature but there appears to be a developmental pattern characterized by vesiculation of the mitochondrial cristae. During early organogenesis, the embryo is in a relative state of hypoxia and this is associated with decrease of terminal electron transport system activity and a marked increase in glycolysis. Ultrastructural studies of a 14 somite monkey embryo, and day 10 and 12 rat embryos, along with a review of the literature led us to determine that this hypoxic stage is characterized by vesiculation of the mitochondrial cristae. Starting in the late morula stage and continuing during early postimplantation embryogenesis the cristae increase and appear tubular or vesicular. After the end of neurulation, and with onset of vascular perfusion, the cristae gradually become lamellated and by the limb bud stage appear more mature. We suggest that new cristae form from blebs of the inner mitochondrial membrane and that subsequently with maturation these blebs collapse giving them a lamelliform appearance. The delamellated state of the cristae may protect the embryo from toxic respiratory end-products of oxidative respiration which could accumulate in an embryo lacking vascular perfusion. In the heart of monkey and rat embryos, the mitochondria had diameters which were approximately twice those found in skin and neural tube. Anat.

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Section: Discussionmentioning

confidence: 54%

Ultrastructural study of mitochondria and their cristae in embryonic rats and primate (N. nemistrina)

1998

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“…For example, rat embryonic heart rates were variably affected by anoxia at E11 (equivalent to mouse E9) but were significantly slowed under the same conditions at later stages (36, 48). In addition, exposure of pregnant mice to hypoxia (8% inspired oxygen) reduced myocardial proliferation, caused myocardial thinning and heart failure, and decreased embryonic survival, particularly at E13.5, while longer exposure (E7.5-E10.5) of early embryos to 10% oxygen had no effect on survival but did decrease embryonic size and myocardial mass at later ages (47, 49).…”

Section: Mitochondria and Bioenergetics During Cardiac Developmentmentioning

confidence: 99%

Bioenergetics, mitochondria, and cardiac myocyte differentiation

Porter

Hom

Hoffman

et al. 2011

Progress in Pediatric Cardiology

132

122

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Cardiac metabolism is finely tuned, and disruption of myocardial bioenergetics can be clinically devastating. Many cardiomyopathies that present early in life are due to disruption of the maturation of these metabolic pathways. However, this bioenergetic maturation begins well before birth, when the embryonic heart is first beginning to beat, and continues into the mature animal. Thus, the changes in energy production seen after birth are actually part of a continuum that coincides with the structural and functional changes that occur as the cardiac myocyte differentiates and the heart undergoes morphogenesis. Therefore, although bioenergetics and mitochondrial biology have not been studied in great detail in the developing heart, bioenergetic maturation should be considered an important component of normal myocyte differentiation. Although events occurring after birth will be discussed, this review will focus on the changes in bioenergetics and mitochondrial biology that coincide with myocyte differentiation and cardiac morphogenesis. The relationship of these changes to the etiology and presentation of cardiomyopathies will be used as a starting point for this discussion. Then, after reviewing cardiac development and mitochondrial biology, the published data on bioenergetics and mitochondrial structure and function in the developing heart will be presented. Finally, the case will be made that mitochondria may be critical regulators of cardiac myocyte differentiation and cardiac development.

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“…Further support for the normality of this relatively hypoxic environment of the early postimplantional stages of embryogenesis comes from the observation that oxygen is toxic to day 10 rat embryos, a finding known for some time (Shepard et al, 1969;New and Coppola, 1970), and it is standard laboratory practice at this early stage to culture explanted rat and mouse embryos in ^10% oxygen Shepard et al, 1998, with permission).…”

Section: Mitochondrial Development During Embryogenesismentioning

confidence: 99%

Mitochondrial ultrastructure in embryos after implantation

2000

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Information on the morphology of mitochondria during embryogenesis is scattered in the literature, but there appears to be a consistent pattern. During early organogenesis, the embryo is in a state of relative hypoxia associated with a major decrease in terminal electron transport system activity and a marked increase in anaerobic glycolysis. Ultrastructural studies of a 14-somite monkey embryo and day 10 and 12 rat embryos, together with a review of the literature, led us to determine that this hypoxic stage is characterized by vesiculation of the mitochondrial inner membranes, or cristae. Starting in the late morula stage and continuing during early postimplantation embryogenesis, the cristae increase but appear tubular or vesicular. After the end of neurulation, and with the onset of vascular perfusion of embryonic tissues, the cristae gradually become lamellated; by the limb bud stage they appear more mature. We suggest that new cristae derive from blebs of the inner mitochondrial membrane and that with maturation these blebs collapse, giving them a lamelliform appearance. The delamellated state of the cristae might inactivate oxidative phosphorylation to protect the embryo from toxic respiratory end-products that could accumulate in an embryo before there is vascular perfusion. Consistent with this hypothesis, mitochondrial diameters in the developing heart of monkey and rat embryos were approximately twice those found in skin and neural tube.

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In vitro study of rat embryos. I. Effects of decreased oxygen on embryonic heart rate

Cited by 26 publications

References 4 publications

Ultrastructural study of mitochondria and their cristae in embryonic rats and primate (N. nemistrina)

Ultrastructural study of mitochondria and their cristae in embryonic rats and primate (N. nemistrina)

Bioenergetics, mitochondria, and cardiac myocyte differentiation

Mitochondrial ultrastructure in embryos after implantation

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