LOBAR INTRACEREBRAL HEMORRHAGE MODEL IN PIGS - RAPID EDEMA DEVELOPMENT IN PERIHEMATOMAL WHITE-MATTER

Citation
Kr. Wagner et al., LOBAR INTRACEREBRAL HEMORRHAGE MODEL IN PIGS - RAPID EDEMA DEVELOPMENT IN PERIHEMATOMAL WHITE-MATTER, Stroke, 27(3), 1996, pp. 490-497
Citations number
48
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
27
Issue
3
Year of publication
1996
Pages
490 - 497
Database
ISI
SICI code
0039-2499(1996)27:3<490:LIHMIP>2.0.ZU;2-6
Abstract
Background and Purpose The mechanisms underlying brain injury from int racerebral hemorrhage (ICH) are complex and poorly understood. To comp rehensively examine pathophysiological and pathochemical alterations a fter ICH and to examine the effects of hematoma removal on these proce sses, we developed a physiologically controlled, reproducible, large-a nimal model of ICH in pigs (weight, 6 to 8 kg). Methods We produced lo bar hematomas by pressure-controlled infusions of 1.7 mt of autologous blood into the right frontal hemispheric white matter over 15 minutes . We froze brains in situ at 1, 3, 5, and 8 hours after hematoma induc tion and cut coronal sections for hematoma assessment, morphological b rain examination, and immunohistochemical and water content determinat ions. Results At 1 hour after blood infusion, ''translucent'' white ma tter areas were present directly adjacent to the hematoma. These marke dly edematous regions had a greater than 10% increase in water content (>85%) compared with the contralateral white matter (73%), and this i ncreased water content persisted through 8 hours. In addition, these a reas were strongly immunoreactive for serum proteins. Intravascular Ev ans blue dye failed to penetrate into the brain tissue at all time poi nts, demonstrating that this serum protein accumulation and edema deve lopment were not due to increased blood-brain barrier permeability. Co nclusions Experimental lobar ICH in pigs models a prominent pathologic al feature of human ICH, ie, early perihematomal edema. Our findings s uggest that serum proteins, originating from the hematoma, accumulate in adjacent white matter and result in rapid and prolonged edema after ICH. This interstitial edema likely corresponds to the low densities on CT scans and the hyperintensities on T-2-weighted MR images that su rround intracerebral hematomas acutely after human ICH.