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The microcirculation is a complex network of resistance and exchange vessels, where perfusion is dependent on numerous factors.
This issue is of paramount interest because nutritive perfusion not only depends upon the morphological properties of the network of exchange vessels, but also on functional parameters such as red blood velocity and distances between exchange vessels (Intaglietta and Zweifach, 1974).
With the recent availability of non-invasive techniques for visualization of the microcirculation in both clinical and experimental settings, there is now persuasive evidence of a dissociation between cardiac output and aortic/arterial pressures and the extent to which flow is delivered to the capillary exchange vessels, specifically in settings of septic shock [ 1, 2].
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Larger non-exchange vessels are shown with continued filling and enlargement especially in striatum.
Additional immersion fixed brain sections showed engorgement of larger non-exchange vessels.
A similar pattern is found in the cortex and striatum where non-exchange vessels (larger than 10 μm) become prominent.
Capillary occlusion leads to shunting of blood to non-exchange vessels with early filling and dilation of the venous system.
Compromised capillary perfusion leads to shunting of blood flow through non-exchange vessels with early filling of the venous system.
Focal regions of cortical followed by striatal capillaries are occluded with shunting to larger non-exchange vessels leading to early filling and dilation of deep cerebral veins.
Additionally, continuity found between larger non-exchange vessels is consistent with shunting and early filling of the venous system found on inspection of whole brain.
In the context of a failing BBB, the increased pressure associated with shunting to non-exchange vessels during encephalopathy likely accounts for hemorrhages in GA1 [ 4, 28].
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