Delayed secondary phase of peri-infarct depolarizations after focal cerebral ischemia: relation to infarct growth and neuroprotection.

摘要: In focal cerebral ischemia, peri-infarct depolarizations (PIDs) cause an expansion of core-infarcted tissue into adjacent penumbral regions reversible injury and have been shown to occur through 6 hr after injury. However, infarct maturation proceeds 24 hr. Therefore, we studied PID occurrence 72 both transient permanent middle artery occlusion (MCAo) via continuous DC recordings in nonanesthetized rats. PIDs occurred average 13 times before reperfusion at 2 then ceased for ∼8 After this quiescent period, activity re-emerged a secondary phase, which reached peak incidence consisted mean 52 over 2-24 This phase corresponded the period maturation; rates growth coincided with changes frequency peaked MCAo, also biphasic pattern 78 events Parameters correlated volumes ischemia models. The role development was further investigated MCAo by treating rats high-affinity NMDA receptor antagonist 8 injury, reduced post-treatment 57% provided 37% neuroprotection. Topographic mapping multielectrode revealed multiple sources initiation patterns propagation. These results suggest that contribute recruitment core even restoration blood flow throughout maturation.