Resuscitation with 100% O(2) does not protect the myocardium in hypoxic newborn piglets.

<bold>Background: </bold>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.<bold>Objective: </bold>To assess porcine myocardial damage from enzyme release during hypoxaemia induced global ischaemia, and subsequent resuscitation with ambient air or 100% O(2). To investigate whether CO(2) level during resuscitation influences myocardial damage.<bold>Design: </bold>Newborn piglets (12-36 hours) were exposed to hypoxaemia by ventilation with 8% O(2) in nitrogen. When mean arterial blood pressure had fallen to 15 mm Hg, or base excess to < -20 mmol/l, the animals were randomly resuscitated by ventilation with either 21% O(2) (group A, n = 29) or 100% O(2) (group B, n = 29) for 30 minutes. Afterwards they were observed in ambient air for another 150 minutes. During resuscitation, the two groups were further divided into three subgroups with different CO(2) levels.<bold>Analysis: </bold>Blood samples were analysed for cTnI, myoglobin, and creatine kinase-myocardial band (CK-MB) at baseline and at the end of the study.<bold>Results: </bold>cTnI increased more than 10-fold (p < 0.001) in all the groups. Myoglobin and CK-MB doubled in concentration.<bold>Conclusion: </bold>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. [ABSTRACT FROM AUTHOR]