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 Hatashita, S. Articles by Hoff, J. T. Search for Related Content PubMed PubMed Citation Articles by Hatashita, S. Articles by Hoff, J. T.

Stroke, Vol 19, 91-97, Copyright © 1988 by American Heart Association

ARTICLES

Biomechanics of brain edema in acute cerebral ischemia in cats

S Hatashita and JT Hoff
Section of Neurosurgery, University of Michigan, Ann Arbor.

We studied whether the biomechanical properties of brain play an important role in the development of early ischemic brain edema in cats with middle cerebral artery occlusion. Brain tissue pressure, tissue compliance, and tissue resistance were measured from the gray matter in the core and the periphery of the middle cerebral artery territory for 6 hours after occlusion. Regional cerebral blood flow and water content were also measured from the same areas. Ventricular fluid pressure was recorded. Tissue pressure rose gradually in the core, where flow was 6 ml/100 g/min, over 4 hours and then stabilized. The pressure gradient measured between edematous tissue and ventricular fluid was 5.3 mm Hg. Tissue resistance increased 1 hour after occlusion when water content increased to 10 mg/g. Later, when water content increased by 40 mg/g, tissue resistance decreased and tissue compliance increased significantly. In the periphery, where flow was 17.6 ml/100 g/min, tissue pressure rose slightly while tissue compliance and tissue resistance did not change within 6 hours. Our data indicate that as ischemic injury progresses, edema fluid accumulates in highly compliant brain parenchyma, then migrates through highly conductive tissue into the cerebrospinal fluid spaces, driven by the hydrostatic pressure gradient between the edematous tissue and the cerebrospinal fluid.

This article has been cited by other articles:

				H. C. Roberts, W. P. Dillon, A. J. Furlan, L. R. Wechsler, H. A. Rowley, N. J. Fischbein, R. T. Higashida, C. Kase, G. A. Schulz, Y. Lu, et al. Computed Tomographic Findings in Patients Undergoing Intra-arterial Thrombolysis for Acute Ischemic Stroke due to Middle Cerebral Artery Occlusion: Results From the PROACT II Trial * Editorial Comment: Results From the PROACT II Trial Stroke, June 1, 2002; 33(6): 1557 - 1565. [Abstract] [Full Text] [PDF]

				A. Arbelaez, M. Castillo, and S. K. Mukherji Diffusion-Weighted MR Imaging ofGlobal Cerebral Anoxia AJNR Am. J. Neuroradiol., June 1, 1999; 20(6): 999 - 1007. [Abstract] [Full Text]

				P. Pantano, F. Caramia, L. Bozzao, C. Dieler, and R. von Kummer Delayed Increase in Infarct Volume After Cerebral Ischemia : Correlations with Thrombolytic Treatment and Clinical Outcome Stroke, March 1, 1999; 30(3): 502 - 507. [Abstract] [Full Text] [PDF]