Study on Pathological Process of Cerebral Venous Circulation Disturbance

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Research on cerebral venous circulation disturbances (CVCD) has been limited partly by the lack of animal models that produce consistent venous infarction. We have reported that raty cortical vein occlusion by a photochemical thrombotic technique is a less invasite, clinically relevant and reproducible model. We here investigated microcirculation after venous occlusion and subsequent brain damage in this model.Experiment-1 : We evaluated changes of the cerebral venous flow pattern by fluorescence angiography, regional cerebral blood flow (rCBF) and cerebral blood volume (CBV) assessed by a modem laser Doppler "scanning" technique, and brain damage histologically in a rat cortical vein occlusion model using a photochemical thrombotic technique. Fluorescence angiographic findings could classify animals into 3 groups : (1)Group A,with a changed venous flow pattern after occlusion (n=12) ; (2)Group B,With an interruption of blood flow and/or a growing venous thrombus (n=5) ; (3)Group C : s … More ham-operated animals (n=5). Extravasation of fluorescein, a massive decrease of rCBF,a short-lasting increase of CBVF and regional brain damage were typical for group B.Cortical CBF mapping revealed a transient hyperperfusion zone with hyperemia surrounding a hypoperfused ischemic core in group B.Experiment-2 : We compared the results of two cortical veins occlusion group (T ; n=7) with those of the single vein occlusion with brain damage group (S ; n=5). rCBF reduction observed in group T,which occurred from 30 min post occlusion, was earlier and greater than decrese in group S from 60 min. Histogram obtained from data of group T demonstrated that local CBF of some locations decreased to a level below the ischemic threshold within 90 min. Six among 7 rats in group T had growing venous thrombus with extravasation of fluorescence and brain damage, and infarction size was bigger in group T than in group S.In conclusion, microciruclation perturbation appears very early following venous occlusion to result in the formation of venous thrombus accompanied by local critical ischemia and severe venous infarction. The extent of vein occlusion reflects the brain damage directly. Based on the results of this study, therapy for CVCD should include the prevention of formation of ongoing venous thrombus and ischemia. Less