The present study was done to establish whether the secondary cerebral energy failure could be reproduced in the newborn piglet subjected to transient global hypoxia-ischemia, and whether the evolution of secondary cerebral energy failure could be monitored by measuring the changes of Cyt aa3 using NIRS. Fifteen anesthetized, ventilated newborn piglets (< 3 day) were divided into 2 groups. Eight of hypoxia-ischemia (HI) group were induced transient HI by breathing 8% oxygen and complete occlusion of bilateral common carotid arteries for 30 min followed by release of occluders and reoxygenation and maintained for up to 48 h. Seven were given sham operation and maintained for 48 h also. Monitoring of cerebral Hb, HbO, HbT and Cyt aa3 were continued throughout the experiment using near infrared spectroscopy. Na+, K(+)-ATPase activity, lipid peroxidation products (conjugated dienes), tissue high energy phosphates (ATP and phosphocreatine) levels and brain glucose and lactate levels were determined biochemically in the cerebral cortex harvested at the termination of experiment. HbT as an index of a cerebral blood volume increased at 2 h after resuscitation significantly in HI group. During hypoxia-ischemia Cyt aa3 fell to -2.0 +/- 0.5 mu l-1 (p < 0.01), returned to baseline on resuscitation, but decreased again progressively from 33 h, and finally fell to -2.2 +/- 0.9 mumol l-1 (p < 0.01) at 48 h in spite of normal physiologic values. There were no changes in control animals. Cerebral level of ATP and PCr in HI group decreased significantly compared to control and ATP concentrations were correlated with the final levels of Cyt aa3. In HI group, cerebral Na+, K(+)-ATPase activity decreased, but the cerebral level of conjugated dienes, glucose, lactate was not different compared to controls. These findings suggest that secondary cerebral energy failure was successfully reproduced in the newborn piglets after transient hypoxia-ischemia and the continuous in vivo NIRS monitoring can be used as a useful tool for the monitoring of delayed cerebral injury.