The effect of isovolemic hemodilution on local tissue oxygen pressure (pO2) and on the power of the electrocorticogram (ECoG) was investigated in the brain of the cat under normal conditions and during focal ischemia. Ischemia, produced by clamping of the middle cerebral artery (MCA) by a transorbital approach, was performed in two series of cats for 2 h. In one group of animals, isovolemic hemodilution was achieved in the second hour of persisting clamping. Local pO2 was continuously recorded on the median ectosylvian gyrus by a multiwire surface electrode. After MCA clamping, local tissue pO2 markedly decreased and hypoxia occurred in the ischemic area. During isovolemic hemodilution until a hematocrit of 20%, local pO2 in the ischemic area did not decrease any further although arterial oxygen capacity was drastically reduced. The power of the ECoG did also not decrease any further in comparison to the situation of ischemia without hemodilution. In the normal brain isovolemic hemodilution until a hematocrit of 20% did not significantly change mean tissue pO2 and the power of the electrocorticogram. We conclude from these results that during isovolemic hemodilution the decreased arterial oxygen capacity is compensated by an increase in microflow in the normal and ischemic region of the brain.