H. Laursen et al., CEREBROVASCULAR PERMEABILITY AND BRAIN EDEMA AFTER CORTICAL PHOTOCHEMICAL INFARCTS IN THE RAT, Acta Neuropathologica, 86(4), 1993, pp. 378-385
The importance of protein extravasation for the development of vasogen
ic brain edema is still controversial.We, therefore, assessed the cere
brovascular permeability to serum proteins in relation to the developm
ent and resolution of brain edema in a photochemical cortical lesion i
n the rat. Cortical infarction was induced by in situ thrombosis using
an argon laser beam aimed at the exposed parietal bone in animals giv
en rose bengal i.v. The histology and the cerebrovascular permeability
to serum proteins were scrutinized from 2 h to 3 weeks after the insu
lt. The presence of serum proteins was demonstrated by an immunoperoxi
dase technique. The cerebral water content was estimated by specific g
ravity measurements of the cortical tissue in a kerosene-monobromobenz
ene gradient column from 2 h to 7 days after infarction. The blood-bra
in barrier was permeable to proteins at 2 h following the insult and p
roteins spread into the medial and lateral tissue reaching a maximum a
t 24 h. The specific gravity did not deviate from control values at 2
h. After 8 h the specific gravity of the lesion decreased with smaller
decreases in the immediately adjacent tissue. At 24 h the changes in
specific gravities reached a maximum in all regions except the immedia
tely lateral area. The edema was generally worse in tissue medial to r
ather than lateral to the infarct. The degradation of serum proteins a
nd the resolution of the brain edema followed the same time course wit
h partial resolution of 72 h. By 1 week serum proteins and edema were
confined to the central necrotic core. The results suggest a relations
hip between cerebrovascular permeability and cerebral edema in photoch
emical cortical infarction.