Mitochondrial Dysfunction and Maturation Phenomenon in Ischemic Gerbil Cortex

Summary

We examined the time course of energy impairment in the cerebral cortex, which develops cerebral infarction after repeated ischemia. Cerebral ischemia was induced in the gerbil by repeated unilateral carotid-artery occlusion (two 10-min periods of ischemia separated by a 5-h interval). Histological examination of the cortex at the stereotaxic levels of chiasma and infundibulum revealed infarction and disseminated selective neuronal necrosis (DSNN), respectively, 7 days after transient ischemia. Cortical glucose content increased at both levels 5 h after the second transient ischemia. At the infundibular level, cortical succinic dehydrogenase (SDH) activity remained within the normal range after ischemia. The cortical activity at the chiasmal level remained within normal range during the initial 12 h. However, the activity gradually reduced thereafter to 28±7.6% of the control level at 2 days of recirculation. The time course of cortical adenosine triphosphate content paralleled the change in SDH. Lactate and tissue pH changes indicated lactoacidosis at the chiasmal level, but not at the infundibular level. Thus, energy metabolism slowly deteriorated over the 2 days of recirculation in the area of the cortex that developed infarction. Mitochondrial dysfunction appears to play a crucial role in the recruitment into the infarction process of postischemic tissue, which is developing DSNN.