Using a newly devised model of dural sinus occlusion, we investigated the pathophysiology of venous haemorrhage as well as venous circulatory disturbance. The superior sagittal sinus (SSS) and diploic veins (DV) were occluded in 16 cats. Intracranial pressure (ICP), cerebral blood volume (CBV) and regional cerebral blood flow (rCBF) were measured for 12 hours after the occlusion. At the end of the experiment, cerebral water content was estimated. In another 8 cats additional occlusions of cortical veins were carried out. In both groups, the blood-brain barrier permeability was evaluated with Evans blue or horseradish peroxidase. The SSS and DV occlusion produced a significant increase in ICP and CBV concomitant with a significant decrease in rCBF. Cerebral water content also increased significantly. However, there was no transition of Evans blue and horseradish peroxidase through the cerebral vessels, and no haemorrhages could be observed. In contrast, the additional occlusion of cortical veins produced haemorrhagic infarctions with Evans blue extravasation in 6 out of the 8 cats. These data suggest that dural sinus occlusion may lead to an increase in CBV and cerebral water content resulting in intracranial hypertension and decreased rCBF. The brain oedema in this model seemed to be mainly hydrostatic oedema, and might also be contributed by cytotoxic oedema. The additional occlusion of cortical veins might be essential in the development of haemorrhage in this model, and the blood-brain barrier was also disrupted in these areas.