TY - JOUR
T1 - Dynamics of cerebral edema. The role of an intact vascular bed in the production and propagation of vasogenic brain edema
AU - Aarabi, B.
AU - Long, D. M.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1979
Y1 - 1979
N2 - Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical technique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; replacement of the frozen brain is unable to induce significant increase in permeability if the surrounding blood-brain barrier or a significant amount of brain edema; and if the lesion is removed at 2,4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.
AB - Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical technique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; replacement of the frozen brain is unable to induce significant increase in permeability if the surrounding blood-brain barrier or a significant amount of brain edema; and if the lesion is removed at 2,4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.
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U2 - 10.3171/jns.1979.51.6.0779
DO - 10.3171/jns.1979.51.6.0779
M3 - Article
C2 - 501422
AN - SCOPUS:0018621428
SN - 0022-3085
VL - 51
SP - 779
EP - 784
JO - Journal of neurosurgery
JF - Journal of neurosurgery
IS - 6
ER -