In lightly anesthetized cats, the left middle cerebral artery was occluded using a transorbital approach. Pial arterial pressure was measured with a feedback-controlled micropressure recording system in the territory of the occluded artery, and compared with changes of cortical blood flow, cortical steady potential and cortical EEG activity. After middle cerebral artery occlusion pial artery pressure fell from 56.2 +/− 1.6 to 7.8 +/− 0.4 mm Hg; during the following two hours it again slowly rose to about 15 mm Hg. Cortical heat conductance, as a measure of blood flow, decreased from 15.1 +/− 0.2 to 11.9 +/− 0.2 × 10(−4) cal × cm-1 × sec-1 × degrees C-1, and remained at this level throughout the observation period. Cortical steady potential shifted by 9.1 +/− 0.7 mV towards negativity, and EEG amplitude was reduced by about 50%. Pial arterial pressure correlated with blood flow, cortical steady potential and EEG amplitude, but not with EEG frequency. Autoregulation and CO2 reactivity of blood flow were disturbed after middle cerebral artery occlusion. Calculation of extra- and intracortical vascular resistances revealed that this disturbance was entirely due to intracortical vasoparalysis whereas the collateral vessels supplying the ischemic territory continued to react to both pressure and CO2 changes. Maintained vascular reactivity of collateral vessels, therefore, is a decisive factor for the efficiency of therapeutic blood flow improvement after acute middle cerebral artery occlusion.