Kr. Wagner et al., LOBAR INTRACEREBRAL HEMORRHAGE MODEL IN PIGS - RAPID EDEMA DEVELOPMENT IN PERIHEMATOMAL WHITE-MATTER, Stroke, 27(3), 1996, pp. 490-497
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.