Free fatty acid (FFA) accumulation during cerebral ischemia has been described as an indicator of ischemic damage. Furthermore arachidonic acid (AA) metabolites, liberated from glycerophospholipids, have been confirmed to induce disturbances of membrane functions. Are there differences in AA levels in the hippocampus of normo- and hypothermic gerbils following ischemia-reperfusion? In an attempt to answer this question, we first studied the time course of changes in the amount of AA liberated from glycerophospholipids using gerbils subjected to 5 min of ischemia-reperfusion under normo- and mild hypothermia. FFAs (including AA) were separated from total lipids by Bond Elut (NH2) column chromatography and analyzed by gas-liquid chromatography. Mild intra-ischemic hypothermia (MIH) did not affect the ischemia-induced AA accumulation following of 5 min of forebrain ischemia. The accumulated AA amounts under MIH tend to decrease more slowly to baseline levels from 15 to 30 min of reperfusion than do the levels under normothermia. These results suggested that MIH reduced the rate of metabolism of AA after reperfusion and might suppress the generation of free radical, eicosanoids and other bioactive metabolites.