Movement of Water Between Blood, Brain and CSF in Cerebral Edema

Summary

Movement of water between blood, brain, and cerebrospinal fluid was studied in cats with experimentally induced brain edema. A freeze lesion was used to induce edema characterized by an increase of brain extracellular space fluid. Major blood vessels supplying blood to the head were clamped to produce edema characterized by an increase of brain intracellular space fluid. Serum osmolality was decreased also to induce intracellular edema. Bulk flow of CSF into the cerebral ventricles was measured by the technique of ventriculocisternal perfusion. After perfusion, the water content of cerebral gray and white matter was measured.

Twenty-four h after the freeze lesion, CSF volume flow rates were not significantly different from normal. Cerebral gray and white matter contents at the center of the lesion were 83.6% and 80.2%, respectively, and were significantly higher than the values measured from the contralateral hemisphere.

After 15 min of ischemia, CSF bulk flow rate was not different than preischemic values. Cerebral gray and white matter water content values were also normal. When the ischemic cats were additionally made hypotensive, cerebral swelling developed and ventriculocisternal perfusion was not possible. Under these conditions there was a significant increase only in gray matter water content.

When water intoxication was induced by i.v. infusion of a 10 mosm sucrose solution (2.2 ml/min for 105 min), decreasing serum osmolality to 275 mosm, bulk flow rate increased to 60 μl/min from a control value of 23 μl/min. Cerebral gray and white matter water contents were 81.2% and 69.7%, respectively, which are significantly greater than normal values of 79.6% and 67.7%. During ventriculocisternal perfusion with a 30 mosm solution, CSF bulk flow was completely inhibited. During simultaneous water intoxication, the volume flow increased to 31 μl/min. When the choroid plexus was or was not inhibited, i.v. infusion of solutions of different osmolality resulted in parallel changes of CSF bulk flow rate. Brain water content did not change, however, unless serum osmolality was altered by at least 10%. These results indicate that the increased flow of fluid into the cerebral ventricles comes from the brain.

Despite the fact that a freeze lesion increases permeability of the blood-brain barrier and edema fluid moves through extracellular spaces, bulk flow of CSF into the ventricles did not change. On the other hand, during water intoxication, with an intact blood-brain barrier and an intracellular shift of water, there is a marked increase in bulk flow of fluid into the ventricles. Our data suggest, however, that under these conditions, this increased fluid flow originated in the brain. There was also evidence to suggest that the preferential flow of fluid into the CSF compartment limits the degree of cerebral edema, i.e., CSF acted as a sink to limit increase in brain water content. Thus, the flow of fluid through the brain may be affected, not only by the osmotic and hydrostatic driving pressures but also by the brain’s resistance to flow. In vasogenic edema, disruption of the blood-brain barrier may change the resistance to flow by altering the extracellular spaces of the brain. This may limit the movement of fluid into the CSF compartment.