Transient elevation of the intracranial pressure increases the infarct size and perifocal edema after subsequent middle cerebral artery occlusion in the rat.
The objective of this study was to mimic in a simple experiment the two major brain insults sustained by the patient with a subarachnoid hemorrhage, that is, the ictus and the subsequent delayed reduction of focal cerebral blood flow caused by vasospasm without the interference of subarachnoid blood, to test the hypothesis that ictal events not related to the presence of blood in the subarachnoid space per se may be important for the development of ischemic deficits and cerebral infarction when vasospasm develops. Groups of rats were subjected to a sudden transient elevation of the intracranial pressure to a level causing a brief period of complete global ischemia by infusion of mock cerebrospinal fluid into the cisterna magna (this manipulation was designed to allow survival of the animal and recovery of consciousness). Two and one-half hours later, a focal ischemic insult was induced by occlusion of the middle cerebral artery. Rats subjected to middle cerebral artery occlusion alone and sham operation served as controls. The infarct size was used as the end point and was calculated on brain slices stained with 2,3,5-triphenyltetrazolium chloride. The study demonstrates that a brief sudden elevation in intracranial pressure, in itself consistent with survival and recovery, increased the vulnerability of the brain to a subsequent focal ischemic insult. Thus the combination of insults resulted in significantly (P less than 0.05) larger infarcts than did middle cerebral artery occlusion alone. Further, this combination of insults resulted in a disproportionate enlargement of the affected hemisphere, which could not be explained by the increased infarct size alone.