C. Nordborg et al., EDEMA-RELATED TISSUE-DAMAGE AFTER TEMPORARY AND PERMANENT OCCLUSION OF THE MIDDLE CEREBRAL-ARTERY, Neuropathology and applied neurobiology, 20(1), 1994, pp. 56-65
Eleven adult spontaneously-hypertensive male rats (SHR) were studied 2
2 h or 7 days after a 2 h unilateral occlusion of the right middle cer
ebral artery (MCA). Another 11 SHR were studied after 24 h or 7 days o
f permanent MCA ligation. The brain infarcts were significantly larger
(P < 0.05) after permanent occlusion than after a 2h occlusion. More
extensive and widespread vasogenic oedema, emanating from the infarcts
, was visualized immunohistochemically in the temporarily-ligated anim
als and the relative number of astrocytes in their contralateral hemis
pheres was greater, thereby indicating that the vasogenic oedema influ
ences the degree of gliosis. An immunopositivity for albumin but not f
or fibrinogen extended via the white matter into the ipsilateral thala
mic nuclei, where cytolytic nerve cell damage, severely shrunken and k
aryorrhectic nerve cells as well as gliosis were found one week after
permanent and temporary MCA ligation. The histological changes in the
thalamus indicated a difference in timing between lateral and medial p
arts of the lesion as well as between temporarily- and permanently-lig
ated SHR. These findings together with the close spatial correlation w
ith albumin immunoreactivity indicate that the spread of extravasated
plasma constituents or degradation products with the oedema bulk flow
from the infarct influences the timing, character and extent of thalam
ic lesions after cerebral infarction.