Effect of middle cerebral artery compression on pial artery pressure, blood flow, and electrophysiological function of cerebral cortex of cat.

In 20 cats, the left middle cerebral artery was gradually compressed with a microdriven vascular occluder implanted by a transorbital approach. Pial artery pressure, cortical blood flow, segmental vascular resistance, electrocorticogram, and cortical steady potentials were measured in the territory of the left middle cerebral artery and correlated with the degree of vascular stenosis. Pial artery pressure began to decrease when the lumen of the middle cerebral artery was reduced to 200 micrometers. Cortical blood flow and EEG power declined when pial artery pressure fell below 35-40 mm Hg; cortical steady potential started to shift toward negativity at a pressure below 25-30 mm Hg; and both hemodynamic and electrophysiological changes were maximal at a pressure below 10 mm Hg. When the vascular occlusion was released within 5 min after the onset of ischemia, a pial artery pressure of only 18 mm Hg was necessary to restore normal blood flow. After 1-h occlusion, normalization of flow occurred at a pressure of 30 mm Hg. Since this pressure is still substantially below normal pial artery pressure, no-reflow does not seem to be of significance in this experimental situation.