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Figure 1 | Experimental & Translational Stroke Medicine

Figure 1

From: Blood brain barrier breakdown as the starting point of cerebral small vessel disease? - New insights from a rat model

Figure 1

Stases, BBB disturbances and microvascular dysfunction in SHRSP. Erythrocyte accumulations (stases) in a capillary (A, hippocampus) and arterioles (B - D, basal ganglia) associated with endothelial injury indicated by beginning diapedesis of erythrocytes (B &C, white arrows) and IgG-deposits within the wall of affected vessels (E &F; E, erythrocyte autofluorescence in magenta). Stases might be the consequence of erythrocyte accumulations (G &H, white arrows) within a mesh of thrombocytes (G) and threads of the von-Willebrand-factor (vWF; H) both activated by blood brain barrier breakdown as illustrated by wall adherence of the vWF in small vessels with IgG deposits (I). Note the disturbed vascular tone in small vessels with stases indicated by sausage-like wall dilatations, here shown in a striatal trifurcation of arterioles (D). E is taken from [25]. AD Hematoxylin Eosin (HE) staining. STL - solanum tuberosum lectin used as endothelial marker, Laminin used as basement membrane marker.

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