The syndrome of hypoxemia-related myocardial dysfunction in the newborn is generally associated with severe intrapartum asphyxia. We investigated the changes in total and regional distribution of myocardial blood flow (MBF) that occur during asphyxia and the factors that regulate MBF, in the chronically prepared, near term, fetal lamb. Studies were done in the awake, physiologically stable state 36–72 h after surgical preparation.In uteroasphyxia was produced by partial cord occlusion and blood flow to fetal organs was measured by the radioactive microsphere technique. A complete set of control measurements was made, and then an occlusion loop was inflated to partially occlude the umbilical vessels. After 30–60 min of partial occlusion, all measurements were repeated. The third set of measurements was made after release of the occlusion loop. Six animals were studied and 17 sets of measurements obtained.Partial umbilical cord constriction produced a progressive asphyxia and acidosis. Cardiac output was severely depressed, although the increase in percentage of cardiac output directed to the myocardium (%F) was very significant. Release resulted in improved cardiac output and O2and CO2exchange, although the metabolic acidosis was worse. No change occurred in the intra-myocardial distribution of MBF during asphyxia or recovery. Total MBF was not significantly increased during asphyxia.Multiple linear regression analysis indicated that arterial oxygen saturation (SaO2) and heart rate were statistically significant predictor variables for absolute MBF, accounting for about 45% of the variation in MBF. Further analysis determined that mean arterial blood pressure, pH, Po2, and Sao2were all statistically significant univariate predictors of MBF as %F, but only Sao2was a statistically significant multivariate predictor, accounting for about 82% of the variation in %F.We conclude that redistribution of a reduced cardiac output during cord occlusion is a major profective mechanism to maintain perfusion of vital organs. This redistribution is due in part to obstruction of placental blood flow, and probably also in part to chemoreceptor mediated circulatory reflexes, via O2receptors. No intramyocardial redistribution of coronary perfusion was observed during asphyxia; thus, this study provides no evidence for regional myocardial ischemia as a complication of severe intrapartum asphyxia.