Abstract
Background: Perinatal asphyxia is associated with cardiac dysfunction secondary to myocardial ischaemia. Cardiac troponin I (cTnI) is a marker of myocardial necrosis. Raised concentrations in the blood are related to perinatal asphyxia and increased morbidity. Objective: To assess porcine myocardial damage from enzyme release during hypoxaemia induced global ischaemia, and subsequent resuscitation with ambient air or 100% O2. To investigate whether CO2 level during resuscitation influences myocardial damage. Design: Newborn piglets (12-36 hours) were exposed to hypoxaemia by ventilation with 8% O2 in nitrogen. When mean arterial blood pressure had fallen to 15 mm Hg, or base excess to < 0.001) in all the groups. Myoglobin and CK-MB doubled in concentration. Conclusion: The considerable increase in cTnI indicates seriously affected myocardium. Reoxygenation with 100% oxygen offered no biochemical benefit over ambient air. CK-MB and myoglobin were not reliable markers of myocardial damage. Normoventilation tended to produce better myocardial outcome than hyperventilation or hypoventilation.
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CITATION STYLE
Børke, W. B., Munkeby, B. H., Mørkrid, L., Thaulow, E., & Saugstad, O. D. (2004). Resuscitation with 100% O2 does not protect the myocardium in hypoxic newborn piglets. Archives of Disease in Childhood: Fetal and Neonatal Edition, 89(2). https://doi.org/10.1136/fn.89.2.f156
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