[Delayed neuronal dysfunction after recirculation of cerebral ischemia]

Delayed neuronal deterioration of recovered neuronal function from cerebral ischemia was investigated in experiments using 25 cats. The neuronal function was evaluated by direct cortical response (DCR) and EEG. To induce cerebral ischemia clamps were applied to both the innominate and left subclavian arteries and were removed 15 minutes after complete loss of DCR. Following recovery of circulation, DCR and EEG were studied for at least 48 hours, along with the changes of cerebral blood flow (CBF) and intracranial pressure (ICP). In 7 of 25 cats CBF gradually or rapidly decreased after it was regained through recirculation due to the increase of ICP, resulting in no recovery of neuronal function. In the other 18 cats normal values of CBF and ICP were observed soon after the recirculation although temporary increase of ICP was found. The recovery of DCR and EEG was observed in 12 of these 18 cats, and these functions were maintained up to the end of the experiment in 9 of these 12 cats. In the other 3 cats and another 5 cats in which only DCR was recovered, these neuronal functions deteriorated 8 to 30 hours after recirculation. In one cat neither DCR nor EEE was recovered at all. Moreover, in the 9 cats mentioned ICP gradually increased before or after the deterioration of neuronal functions, and it finally reached the level of systemic blood pressure. These results indicate that the recovery of neuronal function from ischemic insults must be judged at least 48 hours after recirculation because of delayed neuronal deterioration, and pathogenesis of delayed neuronal dysfunction and delayed increase of ICP must be fully investigated thereafter.