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Related Experiment Video

Updated: Mar 9, 2026

Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema
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Simulating vasogenic brain edema using chronic VEGF infusion.

Martin Piazza1, Jeeva Munasinghe2, Roger Murayi1

  • 1Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, and.

Journal of Neurosurgery
|January 7, 2017
PubMed
Summary
This summary is machine-generated.

Researchers developed a novel model for vasogenic brain edema (VBE) using vascular endothelial growth factor (VEGF) infusion in rats. This model accurately simulates VBE without tumor presence, offering a new tool for studying brain edema mechanisms.

Keywords:
AQP4 = aquaporin-4BBB = blood-brain barrierCI = confidence intervalFITC = fluorescein isothiocyanateFSE = fast spin-echoGFAP = glial fibrillary acidic proteinIPH = intraparenchymal hemorrhagePBS = phosphate-buffered salinePTBE = peritumoral brain edemaROI = region of interestRSA = rat serum albuminVBE = vasogenic brain edemaVEGFVEGF = vascular endothelial growth factoranimal modelbrain edemacannulainfusionperitumoralratvasogenic

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Area of Science:

  • Neuroscience
  • Biomedical Engineering
  • Pathology

Background:

  • Peritumoral brain edema (PTBE) is a significant challenge in neuro-oncology.
  • Vascular endothelial growth factor (VEGF) plays a key role in PTBE by disrupting the blood-brain barrier (BBB).
  • Existing models for studying VBE often involve complex tumor environments or lack detailed validation.

Purpose of the Study:

  • To establish a reliable animal model for vasogenic brain edema (VBE) using chronic VEGF infusion.
  • To validate the VBE model through serial in-vivo MRI and histological analysis.
  • To create a model that excludes tumor-specific factors, focusing solely on VBE mechanisms.

Main Methods:

  • Stereotactic implantation of brain cannulas in male Fischer rats (n=182) for chronic VEGF infusion (2-20 µg/ml).
  • Serial high-field (9.4-T) MRI acquisition at multiple time points (12-144 hours) during VEGF or control infusion.
  • Histological and immunohistochemical analyses of brain tissue to assess BBB integrity, edema volume, and cellular responses.

Main Results:

  • VEGF infusion led to a significant increase in T2 hyper-attenuation (edema volume) compared to controls (42.90 ± 3.842 mm³ vs. 8.585 ± 1.664 mm³).
  • Postcontrast T1 enhancement indicated BBB breakdown in VEGF-infused rats.
  • Histology revealed no necrosis or inflammation, but showed astrocyte activation, vascular remodeling, and increased claudin-5 expression.

Conclusions:

  • Chronic brain infusion of VEGF provides a reliable and reproducible model for VBE.
  • This model effectively simulates VBE without confounding factors like necrosis or inflammation.
  • The VEGF-induced VBE model facilitates precise investigation into edema formation mechanisms and therapeutic strategies.