To explore the effects of reperfusion on evolution of focal ischemic injury, spontaneously hypertensive male rats were subjected to photothrombotic distal middle cerebral artery occlusion (MCAO) with or without YAG laser-induced reperfusion. The volume of fodrin breakdown zone, water content, and brain tissue levels of sodium (Na(+)) and potassium (K(+)) were measured in the ischemic core and penumbra. Reperfusion attenuated fodrin breakdown, and the volume containing fodrin breakdown product at 3 h after reperfusion (5 h after MCAO) (30 +/- 7 mm(3)) was significantly smaller than the 42 +/- 3 mm(3) of the permanent occlusion group. After 3 to 6 h of ischemia, Na(+) increased, and K(+) decreased in the ischemic core. Reperfusion after 2 h of MCA occlusion did not mitigate the ischemia-induced changes in brain tissue electrolytes and water content at 3 to 6 h of ischemia. Even in reperfusion after comparatively long periods of occlusion where brain infarction size, assessed 3 days after MCAO, was not significantly reduced by reperfusion, and the precipitating indicators of the ischemic core (Na(+), K(+), water content) did not improve, temporary improvement or a delay in progression of ischemic injury was discernible in the penumbra. These results indicate the possibility that treatment with reperfusion is permissive to the effects of neuroprotection.