Transport of sodium from blood to brain in ischemic brain edema.

Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of 22Na and [3H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with neurologic symptoms, unilateral carotid occlusion reduced the cerebral blood flow in the ipsilateral cerebral hemisphere to 13 +/- 4 ml/100 g/min (n = 6). The water content of the ischemic hemisphere increased from 79.0 +/- 0.6 to 80.8 +/- 0.2% (n = 7, p less than 0.001) and tissue sodium content increased from 231 +/- 17 to 359 +/- 23 mEq/kg (p less than 0.0001). However, there was a 40% reduction in the sodium permeability-surface area product of the ischemic hemisphere compared with the control side (1.65 +/- 0.44 vs 2.79 +/- 0.29 microliter/g/min, n = 6, p less than 0.001). The sucrose permeability-surface area product, a measure of blood-brain barrier integrity, was unchanged. Although ischemia was less severe in the diencephalon, the tissue water and sodium contents increased significantly on the ischemic side. In contrast to the cerebral hemisphere, however, the permeability-surface area products for both sodium and sucrose were unchanged in the ischemic diencephalon. These results suggest that the increase in tissue sodium seen in ischemic edema is not due to enhanced sodium uptake; we speculate that it results, in part, from a reduction in sodium and water clearance from the tissue.