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Updated: Dec 24, 2025

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Published on: November 21, 2025
Mechanisms of blood-brain barrier breakdown after microembolization of the cat's brain
Insights
Microembolization disrupts the blood-brain barrier (BBB) in cats, allowing protein leakage. This breakdown is not energy-dependent, occurring through mechanisms independent of cellular processes like pinocytosis.
Area of Science:
- Neuroscience
- Pathology
- Vascular Biology
Background:
- The blood-brain barrier (BBB) protects the central nervous system.
- Disruption of the BBB can lead to neurological dysfunction.
Purpose of the Study:
- To investigate the mechanism of BBB disruption following microembolization.
- To determine if BBB breakdown is an energy-dependent process.
Main Methods:
- Unilateral brain microembolization in adult cats using carbonized microspheres.
- Horseradish peroxidase (HRP) tracer administration at different time points relative to fixation.
- Light microscopic examination of HRP extravasation patterns.
Main Results:
- Microembolization induced multifocal BBB disruption to HRP.
- No qualitative differences in HRP extravasation were observed based on tracer administration timing.
- Endothelial vesicles and tubules were present only after in vivo HRP circulation.
Conclusions:
- BBB breakdown following microembolization is not an energy-dependent process.
- Mechanisms like pinocytosis or tubular-endothelial channel formation are not the primary drivers of protein extravasation in this model.
Abstract:
Unilateral microembolization of the cat brain with carbonized microspheres 15 microns in diameter ten minutes (min) before death induced multifocal disruption of the blood-brain barrier (BBB) to horseradish peroxidase (HRP) in nine adult cats. The gross pattern of HRP extravasates was studied: (a) after five min of in vivo circulation, (b) following infusion of HRP immediately before chemical fixation, and (c) following infusion of HRP after 60 min of aldehyde fixation. Examination of the material from the three different experimental groups revealed no qualitative differences at the light microscopic level; specific features such as ring-shaped extravasations of HRP occurred irrespective of the mode of tracer injection. Tracer-filled pinocytotic vesicles and tubular profiles were abundant in the vascular endothelium after in vivo circulation of HRP, but were virtually absent after supravital and postmortem HRP administration. The results suggest that BBB breakdown for proteins after microembolization is not an energy-dependent process mediated by either pinocytosis or tubular-endothelial channel formation.
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