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

Two hydrostatic factors such as acute hypertension and decompressive craniectomy were chosen and assessment was focused on how the hydrostatic pressure gradient altered the cerebrovascular dynamics and metabolism during the process of development of brain oedema. Hydrostatic oedema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, one with craniectomy (Cr+) and the other without craniectomy (Cr-). Animals were sacrificed immediately, 24 and 48 h after the hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow (rCBF) and glucose metabolism (1CGU) were measured by quantitative autoradiographic methods using 14C-iodoantipyrine and 14C-deoxyglucose, respectively. The hypertensive insult produced multifocal lesions stained by Evans blue. In the brains of the Cr- group, there was a transient increase in water content and no significant change of rCBF and 1CGU. In the Cr+ group, the increase in water content was pronounced and continued until 48 h later. In addition, misery perfusion was observed at 24 h after the insult and both rCBF and 1CGU were significantly decreased after 48 h. These results indicate that the increased hydrostatic pressure gradient enhances tissue damage and causes the reopening of blood-brain barrier.