This Study was designed to investigate the effect of Sunkihwalhyul -Tang extract(SHT) 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, and further to determine the mechanisms of action of SHT on hemodynamics. In addition, this study was designed to investigate whether SHT inhibits lactate dehydrog enase(LDH) activity in neuronal cells and cytokines production in serum of cerebral ischemic rats. The results were as follows 1. SHT significantly increased rCBF and PAD in a dose-dependent manner, but MABP was not changed by injecting SHT. These results suggest that SHT significantly increases rCBF by dilating PAD. 2. The SHT-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin(IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase and methylene blue(MTB, $10{mu}g/kg$, i.p.), an inhibitor of guanylate cyclase. 3. The SHT-induced dilation in PAD was significantly inhibited by pretreatment with IDN and MTB. 4. The SHT-induced some increase in MABP was significantly increased by pretreatment with IDN. These results suggest that the mechanism of action of SBT is mediated by guanylate cyclase. 5. Both rCBF and PAD were significantly and stably increased by SHT(10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. 6. SBH significantly inhibited LDH activity in neuronal cells. These results suggest that SHT prevents the neuronal death. 7. In cytokine production in the senlm drawn from femoral artery 1 hr after middlecerebral arterial occlusion, sample group showed significantly decreased production of IL-1$eta$ production, decreased production TNF-$alpha$ and increased Production of IL-10 compared with control group. 8. In cytokine production in the serum drawn femoral artery 1 hr after reperfusion, sample group showed significantly decreased production of IL-1$eta$ and TNF-$alpha$ as wellas significantly increased production of IL10 compared with control group. These results suggest that SHT mediated by guanylate cyclase has inhibitive effect on the brain damage by inhibiting LDH activity, IL-1$eta$ and TNF-$alpha$ production, and by accelerating IL-10 production. The present author thinks that SHT has an anti-ischemic effects through the improvement of cerebral hemodynamics and inhibitive enects on the brain damage.