The effect of transient cerebral ischemia on the vascular permeability to protein tracers

A discrepancy exists between the maintained impermeability of the capillary endothelium to protein tracers and the ultrastructural changes of the endothelial cell cytoplasm following acute ischemia.

Abstract

A study was made on the effect of ischemia on the vascular permeability to proteins in the cat brain. Evans blue and horseradish peroxidase were used as protein tracers. They were intravenously injected and localized by fluorescence and electron microscopy. Acute complete cerebral ischemia produced by arterial ligations for 15 min to 3h did not induce extravasation of the tracers. Electron microscopical observations on the cortical vessels showed that this was due to a maintained barrier function of the vascular endothelium. Incomplete cerebral ischemia of corresponding duration produced by an arteriovenous shunt (between one common carotid artery and one femoral vein) caused exceptionally extravasation around cortical vessels. Some cats with long shunting time showed signs of increased vascular permeability in the thalamus where the tracers had accumulated in neurons. Severe swelling of capillary endothelial and perivascular glial cells and changes of their cytoplasmic organelles were present in animals without signs of increased vascular permeability to proteins. A discrepancy therefore exists between the maintained impermeability of the capillary endothelium to protein tracers and the ultrastructural changes of the endothelial cell cytoplasm following acute ischemia.