Oxygen consumption in the fetal lamb during sustained hypoxemia with progressive acidemia

Rurak, D. W.; Richardson, Bryan; Patrick, John; Carmichael, Lesley; Homan, Jacobus

doi:10.1152/ajpregu.1990.258.5.r1108

Cited by 35 publications

(28 citation statements)

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“…The effects of moderate hypoxia in our study were similar to other reports (13,14,24,25), as were the effects of insulin infusion upon sympathoadrenal, hemodynamic, and metabolic responses of the fetus (6-12, 22, 26).…”

Section: Discussionsupporting

confidence: 91%

Circulatory and Metabolic Effects of Hypoxia in the Hyperinsulinemic Ovine Fetus

1995

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Fetuses of women whose diabetes is poorly controlled often exhibit hypoxemia and elevated catecholamine concentrations at birth. In the ovine fetus, experimental hyperinsulinemia results in hypoxemia, elevated catecholamine concentrations, and hemodynamic changes. Limited oxygen availability occurring during pregnancy-related complications and/or delivery may present an additional risk to the hyperinsulinemic fetus. In this study, we tested the hypothesis that hypoxia induced via acutely limiting oxygen availability compromises the hemodynamically and metabolically stressed but compensated hyperinsulinemic ovine fetus. Fetuses receiving insulin (n = 8) or placebo (n = 5) for 48 h were exposed to maternally induced hypoxia. Hypoxic hypoxia was associated with a surge in catecholamines in the hyperinsulinemic fetuses. During hypoxia, this group exhibited insulinrelated sustained increases in the combined ventricular output and fetal body blood flow, accentuation of the prior insulinrelated increase in blood flow to the heart, decreased systemic oxygen delivery, accentuation of the insulin-related increased oxygen extraction, reductions in the insulin-related increased systemic oxygen uptake, sustained increases in regional oxygen delivery to the heart and adrenal glands, reductions in the insulinrelated increased delivery to the carcass, and decreased oxygen delivery to the kidneys and gastrointestinal tract. We conclude that, in the hyperinsulinemic ovine fetus, hypoxic hypoxia attenuates the hyperinsulinemia-mediated increased systemic oxygen uptake. Regional oxygen transport is preserved to vital regions (brain, heart, and adrenal glands) by increased perfusion and compromised to certain other regions (kidneys and gastrointestinal tract), because the increases in perfusion are insufficient to offset the limited oxygen availability. (Pediatr Res 38: 67-75, 1995) AbbreviationVo,, oxygen uptake Infants born to women with poorly controlled diabetes mellitus have an increased incidence of in utero hypoxemia (I), perinatal asphyxia (2), hypertrophic cardiomyopathy (3, 4), elevated catecholamine concentrations at birth (5), and perinatal mortality, including unexpected sudden fetal death (3). Hyperinsulinemia has been implicated as a major factor in the pathogenesis of many of these morbidities (3). In the ovine fetus, experimental hyperinsulinemia results in hypoxemia (6-12), elevated catecholamine concentrations (11, 12), and hemodynamic changes (6, 9, 11, 12), simulating several of the abnormalities observed in infants of diabetic mothers.Superimposed hypoxia resulting from abruptio placenta, cord entrapment, and/or difficult or prolonged labor and delivery might present an additional life-threatening risk to the hyperinsulinemic fetus. In the ovine fetus, we (12) and others (6) have previously demonstrated that experimental hyperinsulinemia results in increased combined ventricular output, and blood flow to the heart, adrenal glands, gastrointestinal tract, kidneys, and carcass. In contrast, experimental fetal hyp...

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Section: Discussionsupporting

confidence: 91%

Circulatory and Metabolic Effects of Hypoxia in the Hyperinsulinemic Ovine Fetus

1995

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“…This is indicated by an increase in fetal heart rate (by 12.8 Ϯ 4.2 bpm) in combination with añ 5% increase in left pulmonary arterial pressure (23) and has been observed previously during accentuated FBM (21,22). This finding is consistent with previous studies that demonstrated that vigorous FBM impose a significant oxygen demand in the fetus (21) and are commonly associated with increased fetal body movements (24). Indeed, during vigorous FBM, fetal oxygen consumption can increase by 30% (21), and blood flow to the main respiratory muscles (diaphragm and intercostals) increases (22).…”

Section: Discussionsupporting

confidence: 91%

Influence of Fetal Breathing Movements on Pulmonary Hemodynamics in Fetal Sheep

et al. 2004

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During fetal development, pulmonary vascular resistance (PVR) is high, and, as a result, blood flow through the fetal lungs is low. Although PVR markedly decreases at the time of birth, the factors that regulate pulmonary blood flow (PBF) and PVR before and immediately after birth are not clear. Our aim was to examine the relationship between episodes of fetal breathing movements (FBM) and pulmonary hemodynamics during late gestation to further understand the relationship among lung luminal volume, phasic changes in intrapulmonary pressure, and PVR before birth. In chronically catheterized fetal sheep (120 -128 d gestation; n ϭ 5; term~147 d), PBF and PVR were measured during periods of FBM and apnea. Episodes of FBM were divided into periods of accentuated (amplitude of Ͼ3.5 mm Hg change in tracheal pressure) and nonaccentuated periods of FBM. During accentuated episodes of FBM, mean PBF was increased to 159.5 Ϯ 23.4% (p Ͻ 0.0025) of the preceding apneic period and was associated with a 19.1 Ϯ 5.2% reduction in PVR. In addition, during accentuated episodes of FBM, the retrograde flow of blood through the left pulmonary artery was reduced to 90.1 Ϯ 1.0% of the preceding apneic period, which most likely contributed to the increase in mean PBF at this time. Although a change in PBF and PVR could not be detected during nonaccentuated FBM, compared with the preceding apneic period, PBF was linearly and positively correlated with the amplitude (change in pressure) of FBM. We conclude that PVR is decreased and PBF is increased during accentuated episodes of FBM, possibly as a result of phasic reductions in intrapulmonary pressures. At birth, blood flow through the lungs markedly increases as a result of a large reduction in pulmonary vascular resistance (PVR). Although this process plays a vital role in the transition from intra-to extrauterine life, the precise mechanisms involved are still not clear. In particular, it is not clear why PVR is high in the fetus, relative to the newborn. During fetal life, the majority (88%) of right ventricular output bypasses the lungs and is shunted into the systemic circulation via the ductus arteriosus (1). In the late-gestation fetus, the relatively high PVR has been attributed to the low PO 2 of blood perfusing the lungs (2,3), to the balance between vasoconstrictor and vasodilator activity (4 -7), and to the high level of resting lung expansion in the fetus (8).Previous studies have investigated the relationship between lung luminal volume and PVR in the fetus and have shown that PVR is directly proportional to the changes in lung volume, causing pulmonary blood flow (PBF) to cease at total lung capacity (9). Conversely, a reduction in lung liquid volume, to a volume that is equivalent to the end-expiratory lung volume in the air-filled lung after birth, caused a 3-to 4-fold increase in PBF and a substantial decrease in PVR (8). Together, these studies indicate that the degree of lung expansion and the associated change in intraluminal pressure may be important physiologic dete...

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“…With models of maternal hypoxemia (e.g., high altitude or a low inspired oxygen fraction), fetal oxygenation falls while BP rises transiently, but then returns to normal, and then falls below normal [67,68,96,[103][104][105][106]. Perinatal hypoxic-ischemic encepatholpathy models that involve the entire body frequently use umbilical cord occlusion and are accompanied by reduced systemic fetal arterial oxygen tension and content [70,107,108].…”

Section: Pathophysiological Mechanisms Of Wmi Related To the Brachiocmentioning

confidence: 99%

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

et al. 2012

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Despite advances in neonatal intensive care, survivors of premature birth remain highly susceptible to unique patterns of developmental brain injury that manifest as cerebral palsy and cognitive-learning disabilities. The developing brain is particularly susceptible to cerebral white matter injury related to hypoxia-ischemia. Cerebral white matter development in fetal sheep shares many anatomical and physiological similarities with humans. Thus, the fetal sheep has provided unique experimental access to the complex pathophysiological processes that contribute to injury to the human brain during successive periods in development. Recent refinements have resulted in models that replicate major features of acute and chronic human cerebral injury and have provided access to complex clinically relevant studies of cerebral blood flow and neuroimaging that are not feasible in smaller laboratory animals. Here, we focus on emerging insights and methodologies from studies in fetal sheep that have begun to define cellular and vascular factors that contribute to white matter injury. Recent advances include spatially defined measurements of cerebral blood flow in utero, the definition of cellular maturational factors that define the topography of injury and the application of high-field magnetic resonance imaging to define novel neuroimaging signatures for specific types of chronic white matter injury. Despite the higher costs and technical challenges of instrumented preterm fetal sheep models, they provide powerful access to clinically relevant studies that provide a more integrated analysis of the spectrum of insults that appear to contribute to cerebral injury in human preterm infants.

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Oxygen consumption in the fetal lamb during sustained hypoxemia with progressive acidemia

Cited by 35 publications

References 0 publications

Circulatory and Metabolic Effects of Hypoxia in the Hyperinsulinemic Ovine Fetus

Circulatory and Metabolic Effects of Hypoxia in the Hyperinsulinemic Ovine Fetus

Influence of Fetal Breathing Movements on Pulmonary Hemodynamics in Fetal Sheep

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

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