Local cerebral blood flow and glucose metabolism in hydrostatic brain edema.

This study investigated the effect of hydrostatic pressure gradient on the cerebrovascular dynamics and metabolism during the development of brain edema. Hydrostatic brain edema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, with craniectomy (Cr+ group) and without (Cr- group). Animals were sacrificed 0, 24, and 48 hours after hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow and local cerebral glucose utilization were measured by the quantitative autoradiographic method using [14C]iodoantipyrine and [14C]deoxyglucose, respectively. Hypertensive insult produced multifocal lesions stained by Evans blue. Brains from the Cr-group showed a transient increase in water content and no significant change in cerebrovascular dynamics and metabolism. Brains from the Cr+ group showed a pronounced increase in water content which persisted 48 hours later. Misery perfusion was also observed 24 hours after the insult and the cerebrovascular dynamics and metabolism were significantly decreased after 48 hours. These results indicate that an increased hydrostatic pressure gradient enhances tissue damage and causes reopening of the blood-brain barrier.