Substrate metabolism in the developing heart

Ascuitto, R.J.; Ross-Ascuitto, Nancy

doi:10.1016/s0146-0005(96)80068-1

Cited by 70 publications

(57 citation statements)

References 94 publications

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“…In a variety of studies, it has been shown that the neonatal heart has a decreased capacity to oxidize fatty acid [1,[3][4][5]. Nevertheless, in our experiments, when perfusion conditions corresponding to normal oxygen availability were restored following hypoxia and tachycardia, the piglet hearts exhibited enhanced aerobic utilization of exogenously supplied palmitate and generated higher than normal (baseline) rates of 14 CO 2 production from 14 C-labeled palmitate.…”

Section: Discussionmentioning

confidence: 49%

“…An understanding of neonatal heart responses to oxygen insufficiency is important, inasmuch as these hearts are known to be undergoing a transition toward aerobic utilization of substrate for energy production [1][2][3][4][5]. Impaired oxygen availability may cause derangements in cardiac contraction and relaxation and in myocardial oxidative metabolism [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…Impaired oxygen availability may cause derangements in cardiac contraction and relaxation and in myocardial oxidative metabolism [5][6][7][8]. Information about alteration in these energy-requiring and energy-producing processes provides a basis for developing clinical strategies to improve performance of neonatal hearts compromised by a lack of oxygen.…”

Section: Introductionmentioning

confidence: 99%

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Performance of the Neonatal Pig Heart Subjected to Oxygen Insufficiency

Tede²,

Ross-Ascuitto³

et al. 2004

Neonatology

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Isolated, paced, isovolumically beating, neonatal pig (n = 32) hearts underwent retrograde aortic perfusion with a solution containing insulin (100 µU/ml), glucose (5.5 mM), and palmitate (0.55 mM). Glycolysis, lactate release, glucose oxidation, palmitate oxidation, and oxygen consumption were assessed. The hearts were perfused during three periods: (1) baseline, pO₂ ≈ 500 mm Hg, heart rate 150 bpm; (2) hypoxia, pO₂ ≈ 60–80 mm Hg, heart rate 150 bpm, or tachycardia, pO₂ ≈ 500 mm Hg, heart rate 300 bpm, and (3) recovery, return to baseline conditions. For hypoxia and tachycardia, the oxygen supply-demand ratio was comparable (≈1 nmol O₂/mm Hg/g_dry). During baseline, the left ventricular peak systolic pressure (PSP) averaged 126 ± 6 mm Hg, the end-diastolic pressure (EDP) 5 mm Hg, and the relaxation time constant (Tau) 34 ± 2 ms; the coronary flow was 36 ± 2 ml/min/g_dry. During hypoxia, the PSP decreased to 70 ± 2 mm Hg, while EDP, Tau, and coronary flow increased to 26 ± 2 mm Hg, 104 ± 14 ms, and 70 ± 2 ml/min/g_dry, respectively; palmitate oxidation and oxygen consumption decreased well below baseline. During tachycardia, the PSP decreased to 88 ± 1 mm Hg, and the EDP increased to 11 ± 1 mm Hg, while Tau and coronary flow did not change significantly; palmitate oxidation and oxygen consumption increased above baseline. For both stressors, the predicted lactate release underestimated the measured values by a factor of ≈2, but were comparable during baseline and recovery. Upon recovery, PSP returned to ≈80% of baseline, while EDP remained elevated, for both stressors. Glucose oxidation returned to baseline, but palmitate oxidation became accelerated. We conclude for neonatal pig hearts subjected to oxygen insufficiency: (1) that PSP decreases and (2) that EDP and Tau increase with hypoxia, whereas EDP increases, while Tau remains unchanged with tachycardia. Following both stressors, palmitate oxidation becomes enhanced and dissociated from mechanical activity.

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Section: Discussionmentioning

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Performance of the Neonatal Pig Heart Subjected to Oxygen Insufficiency

Tede²,

Ross-Ascuitto³

et al. 2004

Neonatology

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“…Furthermore, insulin has positive inotropic effects (8) independent of glucose metabolism (9) and has been suggested as a treatment for heart failure (HF) (10). Whereas insulin is known to improve neonatal cardiac function (11), the fetal heart has previously been considered resistant to insulin (5).…”

mentioning

confidence: 99%

Glucose-insulin infusion improves cardiac function during fetal tachycardia

Schmidt

Kristiansen

White

et al. 2004

Journal of the American College of Cardiology

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“…ATP generation via these relative oxygen-sparing glycolytic pathways rather than fatty acid oxidation (FAO) represents a key strategy of the fetal heart to tolerate and thrive despite low oxygen levels in normal fetal life [ 14 ]. This adaptive feature allows the fetal heart to be more resistant to hypoxia-induced cell injury than the adult heart [ 15 ]. Expression of hypoxia-induced genes, such as hypoxia inducible factor (HIF-1) and vascular endothelial growth factor (VEGF) play central roles in modulating myocyte development, myocardial angiogenesis, and fetal heart remodeling [ 16 , 17 ].…”

Section: Oxygen Tension Metabolism and Substrate Utilizationmentioning

confidence: 99%

The Neonatal Transition of the Right Ventricle

Maria

2014

The Right Ventricle in Health and Disease

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Substrate metabolism in the developing heart

Cited by 70 publications

References 94 publications

Performance of the Neonatal Pig Heart Subjected to Oxygen Insufficiency

Performance of the Neonatal Pig Heart Subjected to Oxygen Insufficiency

Glucose-insulin infusion improves cardiac function during fetal tachycardia

The Neonatal Transition of the Right Ventricle

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