| ABSTRACT In this paper, the antihemorrhagic cerebral apoplexy effect of YXK was studied by using the model that experimental cerebral hemorrhage in rats. And the action mechanism of YXK to plexy was revealed. T抧e results showed that the formation of thrombus in vivo was dose-dependently inhibited by YXK. YXK can alleviate the vascular permeability, cerebral edema and brain tissue lesion and possess prophylactic and therapeutic effect on hemorrhagic damage of brain tissue. YXK could increase distinctly the contents of 6-keto-PGF1,. and decrease that of tbromboxane A2. But HT could inhibite both of them. Y7XK is able to reduce obviously the dead rate of experimental cerebral hemorrhage rats due to injected auto blood. It also prolong the duration of gasping in rats after complete brain ischemia. Biochemical tests showed that YXK at high dose (8.Og/kg) can enhance the activity of SOD and GSH-Px in the brain tissue and suppress the level of MDA there. So it has powerful functions as follows: scavenging free radical and antioxidation injuring. Blood rheology tests showed that YXK can regulate PFC and plasma viscosity and reduce Hct and ESR. YXK can dose-dependently inhibite the platelet agglutination induced by ADP and AA. The chronic toxicity test was performed by oral administration at the doses of 3.2 and 3S.E g/kg/d for 2 months. No obvious toxicity was found, so the big dose (3B.5glkgld)was considered as the safe dose. The results indicated that YXK is a potent antiplexy. Its mechanism is complex, 3 ABSTRACT which maybe involved in directly improving the blood rheology and cleaning free radical so as to the damage was released, invoving the platelet agglutination. YXK inhibited the platelet agglutination by regulating synergically PGI2/TXA2 to inhibinate the thrombus formation.
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