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The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction
C Nordborg1, T E Sokrab, B B Johansson
1Department of Pathology I, University of Göteborg, Sweden.
Acta Neuropathologica
|January 1, 1991
Summary
Plasma proteins like albumin spread from stroke-induced brain infarcts, causing damage in distant white matter and thalamus, particularly in spontaneously hypertensive rats (SHR). This highlights how protein leakage impacts remote brain injury after cerebral infarction.
Area of Science:
- Neuroscience
- Pathology
- Cerebrovascular Research
Background:
- Cerebral infarction, or stroke, involves blood-brain barrier disruption.
- Understanding the spread of plasma proteins after stroke is crucial for predicting secondary brain damage.
Purpose of the Study:
- To investigate the spatiotemporal dynamics of extravasated plasma proteins (albumin and fibrinogen) after middle cerebral artery occlusion (MCAO) in rats.
- To correlate protein extravasation with remote tissue damage, particularly in the thalamus.
Main Methods:
- Immunohistochemistry was used to detect extravasated albumin and fibrinogen in rat brain sections.
- Middle cerebral artery ligation was performed in normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).
- Coronal brain sections were analyzed at various time points post-ligation (6 hours to 3 weeks).
Main Results:
- Infarcts occurred in all SHR and 6/14 WKY rats.
- Extravasated proteins initially localized to infarct borders, then spread into white matter over time.
- Albumin, but not fibrinogen, extended into thalamic nuclei, correlating with nerve cell damage and gliosis.
Conclusions:
- Extravasated plasma proteins, especially albumin, propagate from cerebral infarcts.
- This propagation, occurring via white matter, contributes to remote thalamic injury and gliosis.
- Plasma protein spread influences the extent and nature of secondary brain damage following ischemic stroke.