TRANSITION FROM ISCHEMIC NEURONAL NECROSIS TO INFARCTION IN REPEATED ISCHEMIA

To study morphological changes in the cortex that follow repeated isch emia, one, two, and three 7-min unilateral occlusions of the carotid a rtery at 6-h intervals, and three, four, and five 7-min similar occlus ions at 12-h intervals were produced in gerbils. Animals with one and two 7-min occlusions at 6-h intervals showed selective neuronal necros is in the cortex; those with three 7-min occlusions at 6-h intervals s howed focal infarction in the third layer of the cortex. Animals with three 7-min occlusions at 12-h intervals showed selective neuronal nec rosis; those with four 7-min occlusions at 12-h intervals showed focal infarction in the third layer. In animals with five 7-min occlusions at 12 h intervals, infarction affecting all layers of the cortex was s een. Results of the present study indicate that cortical infarction oc curred when a brief ischemic insult that does not cause any visible mo rphological damage in cortical neurons was inflicted repeatedly, and t hat development of infarction in the cortex following repeated episode s of ischemia depended on both the number of insults and the time inte rvals between them. This finding suggests that there is a threshold of infarction in repeated ischemia. In our model, various stages of isch emic brain injury could be achieved more easily than in transient isch emia by altering the number of insults or the intervals between them. This model is suitable for studying the pathophysiology on transition from ischemic neuronal necrosis to infarction.