Objectives : This study was designed to investigate the effects of Jayun-tang extract (JYT) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats, na to determine the mechanisms of action of JYT. Methods : We investigated whether JYT inhibits lactate dehydrogenase activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. Results : 1. JYT significantly increased rCBF and PAD in a dose-dependent manner, but MABP was not changed by injecting JYT. These results suggested JYT significantly increased rCBF by dilating PAD. 2. The JYT-induced increase in rCBF was significantly inhibited from pretreatment with indomethacin (1mg/kg, i.p.), an inhibitor of cyclooxygenase and methylene blue $(10{mu}g/kg, i.p.)$, an inhibitor of guanylate cyclase. 3. The JYT-induced dilation in PAD was significantly inhibited from pretreatment with indomethacin, but was increased by pretreatment with methylene blue. 4 The JYT-induced increase in MABP was reduced by pretreatment with indomethacin and methylene blue. 5. JYT significantly inhibited lactate dehydrogenase activity in neuronal cells. These results suggest that JYT prevented the neuronal death. 6. Both rCBF and PAD were significantly and stably increased by JYT $(10{mu}g/kg,;i.p.)$ during the Period or cerebral reperfusion, which contrasted with the findings of rapid and marked increase in the control group. 7. In cytokine production in the serum drawn from femoral artery 1hr after middle cerebral artery occlusion, the sample group showed significantly decreased production of $IL-1eta$ and $TNF-alpha$ as well as increased production of IL-10 and $TGF-eta$ compared with rho control group. 8. In cytokine production in the serum drawn from femoral artery 1hr after reperfusion, the sample group showed significantly decreased production of $IL-1eta$ and $TNF-alpha$ as well as significantly increased production of IL-10 and $TGF-eta$ compared with the control group. Conclusions : JYT mediated by cyclooxygenase had an inhibitive effect on brain damage by inhibiting lactate dehydrogenase activity, $IL-1eta$ and $TNF-alpha$ production, and by accelerating IL-10 and $TGF-eta$ production. The author feels that JYT had anti-ischemic effects through the improvement of cerebral hemodynamics and inhibitive effects on brain damage.