Abstract
Cerebral venous infarction represents an often under diagnosed cause for acute or slowly progressive neurological deterioration. The underlying pathophysiological basis is not well understood, but seems to differ from that of arterial infarction, reflecting the different anatomical and physiological features of the cerebral venous system. The blood-brain barrier (BBB) is the regulated interface between the peripheral circulation and the central nervous system. Dysfunction of the BBB is a characteristic finding in common neurological
disorders and has been shown recently to underlie neuronal dysfunction. In the present study we establish a rat model for venous infarction and investigate the
effects of such pathology on vascular permeability and neuronal functions.
Methods: The open cranial window method was used in anesthetized rats. Cortical vein infarction was induced by photoactivation of Rose bengal via laser-optic illumination. For BBB permeability and cellular injury assessment, sodium
fluorescein and propidium iodide were injected (respectively) intravenously before and following photothrombosis. High frequency (30/s) images were acquired during injection using a CCD camera to allow for the quantification of dye leakage. Image analysis was performed offline using home-made
Matlab scripts.
Results: Pixel-permeability maps reveal that venous infarction induces a gradual spread and increase in BBB permeability over time (30 , 60, 120 and 180 min). In addition BBB permeability was found to be associated with cell damage as
noted using propidium iodide.
Conclusions: We demonstrate that selective venous infarction is associated with gradual increase in vessel permeability in the surrounding cortex, despite the lack of increased intracranial pressure or reduced perfusion. We confirmed that BBB dysfunction is associated with cellular injury. On-going studies are performed to underscore the mechanisms underlying cellular injury and their functional significance.
disorders and has been shown recently to underlie neuronal dysfunction. In the present study we establish a rat model for venous infarction and investigate the
effects of such pathology on vascular permeability and neuronal functions.
Methods: The open cranial window method was used in anesthetized rats. Cortical vein infarction was induced by photoactivation of Rose bengal via laser-optic illumination. For BBB permeability and cellular injury assessment, sodium
fluorescein and propidium iodide were injected (respectively) intravenously before and following photothrombosis. High frequency (30/s) images were acquired during injection using a CCD camera to allow for the quantification of dye leakage. Image analysis was performed offline using home-made
Matlab scripts.
Results: Pixel-permeability maps reveal that venous infarction induces a gradual spread and increase in BBB permeability over time (30 , 60, 120 and 180 min). In addition BBB permeability was found to be associated with cell damage as
noted using propidium iodide.
Conclusions: We demonstrate that selective venous infarction is associated with gradual increase in vessel permeability in the surrounding cortex, despite the lack of increased intracranial pressure or reduced perfusion. We confirmed that BBB dysfunction is associated with cellular injury. On-going studies are performed to underscore the mechanisms underlying cellular injury and their functional significance.
| Original language | English |
|---|---|
| Pages (from-to) | S44 |
| Journal | Journal of Molecular Neuroscience |
| Volume | 53 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1 Aug 2014 |