This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lo, W. D. Articles by Hoff, J. T. Search for Related Content PubMed PubMed Citation Articles by Lo, W. D. Articles by Hoff, J. T.

Stroke, Vol 18, 150-157, Copyright © 1987 by American Heart Association

ARTICLES

Transport of sodium from blood to brain in ischemic brain edema

WD Lo, AL Betz, GP Schielke and JT Hoff

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.

This article has been cited by other articles:

				Y. Wang, W. Hu, A. D. Perez-Trepichio, T. C. Ng, A. J. Furlan, A. W. Majors, S. C. Jones, and E. C. Haley Jr Brain Tissue Sodium Is a Ticking Clock Telling Time After Arterial Occlusion in Rat Focal Cerebral Ischemia Editorial Comment Stroke, June 1, 2000; 31(6): 1386 - 1392. [Abstract] [Full Text] [PDF]