Abstract

Dural sinus occlusion is an infrequent but potentially devastating cause of stroke. The pathophysiological course of events underlying it is, as yet incompletely understood. In a cat model, regional cerebral blood flow (CBF) was measured during control and 2, and 24 hours after superior sagittal sinus occlusion. Around 48 hours after superior sagittal sinus occlusion, experimental settings were terminated by perfusion fixation with 4% paraformaldehyde solution, and haematoxylin and eosin histology. CBF was significantly reduced over the time-period of measurement (p < 0.05) covering about 45% of the brain in planes that were affected by occlusion. Histologically, in all cases signs of subacute venous infarction could be demonstrated. Based on the newly-developed model of microsurgical ligation of the superior sagittal sinus in cats, we present for the first time an animal model for cerebral venous infarction that leads to a histologically proven subacute venous infarction with a good reproducibility. The further advantage of this model is the fact that it mimics the clinical situation as far as possible by its inter- and intra-individual variance of extension of the venous infarction and by the slow reduction of CBF over 24 hours. Sequential PET imaging is a favourable, non-invasive method to gain further insight into the pathophysiological characteristics of experimental cerebral venous infarction. Therefore, the new-developed cat-model as demonstrated in this study will be of great value for further and more detailed investigations of cerebral-venous infarctions, and for the experimental evaluation of therapeutic strategies.

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