A canine model of intracranial arteriovenous shunt with acute cerebral venous hypertension.

Increased pressure of draining veins in intracranial arteriovenous fistula is considered an important cause of clinical symptoms. To investigate hemodynamic changes in intracranial arteriovenous fistula with cerebral venous hypertension, we developed a new canine model of this condition. A lingual artery-superior sagittal sinus (SSS) shunt was constructed using a section of the femoral artery as an interposed graft; immediately after which, monitoring of SSS pressure (SSSP) and regional cerebral blood flow (rCBF) was started. The baseline SSSP was 4.1 +/- 3.7 mmHg. After shunt opening, it increased slightly but not significantly. When the SSS was occluded with a clip with the shunt closed, SSSP rose to 20.3 +/- 9.0 mmHg (p < 0.01). Finally, on shunt opening, with the SSS caudal (downstream) to it occluded, the SSSP increased to 59.5 +/- 22.9 mmHg (p < 0.01, multiple analysis of variance, contrast). The frontal lobe rCBF decreased as the cerebral perfusion pressure (CPP) (mean blood pressure minus SSSP) fell. However, cerebral vascular resistance decreased significantly and proportionately to the reduced CPP (r = 0.66, p < 0.0001). In conclusion, when an intracranial arteriovenous shunt was present, venous outflow obstruction was shown to be necessary for cerebral venous hypertension to occur. In acute venous hypertension, decreases in rCBF occurred, but the autoregulatory vasodilating response was also active.