Biomechanics of brain edema in acute cerebral ischemia in cats.
Shizuo Hatashita, J. T. Hoff
Abstract
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Shizuo Hatashita, J. T. Hoff
Abstract
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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.
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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.
Key concepts: Medicine, Tissue fluid, Ischemia, Edema, Hydrostatic pressure, Compliance (psychology), Brain tissue, Parenchyma