Myocardial necrosis may occur in infants dying after severe asphyxia. The aim of the present study was to determine if myocardial injury occurs in fetuses that survive severe intrauterine asphyxial events. Asphyxia was induced in 12 near-term fetal lambs, by brief, repeated umbilical cord occlusions, continued until severe (<20 mmHg) or sustained hypotension occurred. Sham asphyxia was performed in 8 fetuses. Repeated umbilical cord occlusions led to a severe metabolic acidosis (pH 6.84±0.09, lactate 14.1±1.5 mM, after 128±38 min), with increasing hypotension during occlusions after the first 30 minutes. After the initial recovery period, the mean arterial blood pressure in asphyxiated fetuses remained significantly lower than both baseline and control values for up to 24 hours. The fetal hearts were perfusion fixed 3 days after asphyxia. No evidence of myocardial necrosis was found on light and electron microscopic examination. In the endocardium of both the right and left ventricles, and in the papillary muscles there was dilation of sarcoplasmic reticulum, margination and clumping of nuclear chromatin, and mitochondrial swelling, with reduced matrix density and disorganised cristae. The most severe morphological changes were found in the fetuses with delayed recovery of fetal heart rate after the final occlusion, while the degree of hypotension during occlusions was not significantly related to the severity of changes. Similar transient impairment of myocardial contractility after brief ischemia, without cell death, has been term `stunning'. These data suggest that reversible myocardial injury contributes to cardiac dysfunction during and after perinatal asphyxia.