Metabolic changes in rats with photochemically induced cerebral infarction and the effects ofbatroxobin were investigated 1,3,5 and 7 days after infarction by means of magnetic resonanceimaging (MRI),~1H-and ~(31)p-magnetic resonance spectroscopy(MRS).A region of T_2 hyperintensitywas observed in left temporal neocortex in infarction group and batroxohin group 1,3,5 and 7 daysafter infarction.The volume of the region gradually decreased from 1 day to 7 days after infarction.The ratio of NAA/Cho+Cr in the region of T_2 hyperintensity in the infarction group was significantlylower than that in the corresponding region in the sham-operated group 3,5 and 7 days afterinfarction respectively(P<0.05).Lac appeared in the region of T_2 hyperintensity in the infarctiongroup 1,3,5 and 7 days after infarction,but it was not observed in the corresponding region insham-operated group at all time points.Compared with the sham-operated group,the ratios ofβATP/PME+PDE and PCr/PME+PDE of the whole brain in the infarction group were significantlylower 1,3 and 5 days after infarction respectively(P<0.05),and the ratio of βATP/PCr also wassignificantly lower 1 day after infarction(P<0.05).Batroxobin significantly decreased the volume ofthe region of T_2 hyperintensity 1 and 3 days after infarction(P<0.05),significantly increased the ratioof NAA/Cho+Cr in the region 5 and 7 days after infarction(P<0.05),significantly decreased theratios of Lac/Cho+Cr and Lac/NAA in the region 5 and 7 days after infarction(P<0.05),andsignificantly increased the ratios of βATP/PME+PDE and βATP/PCr in the whole brain 1 day afterinfarction(P<0.05).The results indicated that the infracted region had severe edema,increased Lacand apparent neuronal dysfunction and death,and energy metabolism of the whole brain decreasedafter focal infarction,and that batroxobin effectively ameliorated the above-mentioned abnormalchanges. Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1,3,5 and 7 days after infarction by means of magnetic resonance imaging (MRS), ~ 1H-and ~ (31) p-magnetic resonance spectroscopy .A region of T_2 hyperintensitywas observed in the left temporal neocortex in infarction group and batroxohin group 1,3,5 and 7 daysafter infarction.The volume of the region gradually decreased from 1 day to 7 days after infarction.The ratio of NAA / Cho + Cr in the region of T 2 hyperintensity in the infarction group was significantlylower than that in the corresponding region in the sham-operated group 3,5 and 7 days afterinfarction respectively (P <0.05) .Lac was in the region of T_2 hyperintensity in the infarctiongroup 1,3,5 and 7 days after infarction, but it was not observed in the corresponding region insham-operated group at all time points. Compared with the sham-operated group, the ratios of βATP / PME + PDE and PCr / PME + PDE of the whole brai (P <0.05), and the ratio of βATP / PCr also wassignificantly lower than 1 day after infarction (P <0.05) .Batroxobin significantly decreased the volume of the region of Significant decreased the ratio of NAA / Cho + Cr in the region 5 and 7 days after infarction (P <0.05), significantly decreased theratios of Lac / Cho + Cr and Lac / NAA in the region 5 and 7 days after infarction (P <0.05), and statistically significantly increased the ratios of βATP / PME + PDE and βATP / PCr in the whole brain 1 day after infarction (P <0.05). The results indicated that the infracted region had severe edema, increased Lacand apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormalchanges.