The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction

Abstract

Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.

Glial Fibrillary Acidic Protein in the Cerebrospinal Fluid of Patients with Dementia

“…those with VAD or SDAT, had disorders at the vascular level [19,[52][53][54][55][56]. Extravasation of plasma proteins has previously been associated with the appearance of astrogliosis in ani- 270 Dementia 1996;7:267-272 W allin/Blennow/Rosengren ■ mal models of vascular brain disease [57], This phenome non gives a plausible explanation for the linkage observed in our study between GFAP levels and the albumin ratio. In summary, increased concentrations of CSF-GFAP were observed in AD and VAD, which may support the view that there is an association between the CSF-GFAP level and astrogliosis, the latter known to exist in these diseases.…”

Injury of the Blood Brain Barrier and Up-Regulation of ICAM-1 in Polymicrobial Sepsis

“…This result corresponds to other publications, describing albumin extravasation in toxin-induced rats already after 1 h with a maximum after 24 h after induction of sepsis [32]. Albumin extravasation correlates with cerebral tissue changes after cerebral infarction in rats [33] and seems to be a marker for damage in the central nervous system. In a model of experimental meningitis TNF-␣ being a key cytokine of the septic pathway is associated with the extravasation of albumin across the bloodbrain barrier into the CNS [34].…”

Loss of immunoreactivity for glial fibrillary acidic protein (GFAP) in astrocytes as a marker for profound tissue damage in substantia nigra and basal cortical areas after status epilepticus induced by pilocarpine in rat

“…An additional aspect is that areas of tissue damage are outlined by massively enhanced staining with both polyclonal and monoclonal GFAP antibodies in reactive astrocytes. The same type of demarcation of a lesioned area is seen after ischemic infarction (Chiamulera et al, 1993;Fredricksson et al, 1988;Futrell et al, 1991;Nordborg et al, 1991;Schmidt-Kastner et al, 1993a).…”