By the ligation of gerbils bilateral carotid arteries and then reperfusion, the effects of PFEM and SOD on the stroke index were evaluated after a 45 min cerebral ischemia followed by a 6 hr reperfusion period and on the mortality after a 24 hr reperfusion period. The resulta indicated that both PFEM and SOD could decrease the stroke index and mortality dramatically. We speculated upon the protective effect of PFEM on cerebral damage following ischemia with reperfusion. It might be due to the inhibition of the free radical metabolism.

CPK activity in mitochondria of brain cells was increased following 15 and 30 minutes of ischemia,by four-vessel occlusion in ten monkeys.It sugested that there was a compensatory elevated degradation of energy-rich phosphate during ischemia.while the energy-rich phos- phate degradation was exhausted as ischemia duration extended.At 60 minutes of ischemia the activity of CPK was fallen.Isocittate dehydrogenase activity in mitochondria of brain cells was declined,the more ischemic duration extended,the more the activity decreased. LDH activity in the brain cells was raise after onset ischemia and then diminished.cAMP content in cerbral cortex was decreased after 15 minutes of ischemia,whilst it elevated after 30 minutes of ischemia.The possible mechanism of changes mentioned above was discussed.

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Arterial thrombosis was produced in rats by the electric stimulation of the common carotid artery. Tongmai Wan injections were given at a dosage level of 1mi/100g to the experimental group, and the control group was given normal saline. The results showed that the duration from the electric stimulation of the common carotid artery to the occurrence of obstructive thrombosis in the experimental groups (38.00?4.35min, 38.67?3.8min) was much longer than that in the control groups (23.00?3.67min, 23.00?3.00 min),p

Exposure of gerbils 120 min to a high concentration oxygen (HCO)atmosphere after 60 min cerebral ischemia resulted in a marked increase in cerebral malondialdehyde (MDA, 4.39?0.26 nmol/mg protein). Much less cerebral MDA was among the other groups (2.63?0.50 nmol/mg protein in sham-operated controls; 3.07?0.52 nmol/mg protein in gerbils exposed to HCO without ischemia; 2.96?0.41nmol/mg protein in ger. bils subjected to 60 min ischemia; 2.79?0.59nmol/mg protein in gerbils subjected to 60 min ischemia and 120 min reperfusion). The contents of cerebral water, sodium, increassd after 60 mln cerebral ischemia. The contents of TXB_2 increased, 6-Keto-PGF_(1?) decreased, the elevation of cerebral water and sodium were more obvious after 120 min repefusion following ischemia. There was no difference in these items except for MDA between the reperfusion groups within air and within HCO.The authors proposed the mechanism that HCO elevates the contents of cerebral MDH might be due to abnormal function of election transport chain of mitochondria.

DND in the gerbil hippocampus was performed by bilateral occlusion of carotid arteries for 20 min followed by reperfusion 2 or 7 days. The contents of Ca~(2+) and MDA in drosal hippocampus were measured after two days reperfusion. Neuronal density in CA1 sector of hippocampus was used as an parameter. Effects of nimodipine and Superoxide dismutase (SOD) on DND in hippocampus were observed after 7 days reperfusion.The results indicated that the levels of Ca~(2+) and MDA were increased significantly. DND in hippocampal CA1 sector was ameliorated by both nimodipine and SOD significantly. It was suggested that Ca~(2+) and Iipid peroxidation play an important role in the development of DND hippocampus after transient forebrain ischemia in gerbils. Calcium Antagonist and free radical scavenger have obvious protective effects on DND in hippocampus.

Experimental DIC model was performed by infusion of thrombin and PAMBA. The rate of glomerular microthrombosis was declined from 56% of the control group to 26% of the treated 2h after venous injection of defibrinogenase. The reduction of pletelet count of the treated group (7.9 ?1.17) was more less than the control ( 3.1? 1.44). There was a trece content in plasma fibrinogen 1h after giv ing drug.It was a significant difference bet-ween the treated and control group (P

Acute in-complete cerebral ischemia were induced in 39 rabbits by hypotension coupled with hypoperfusion for 60 min, and acute forebrain ischemia were induced in other 15 rabbits by 4A-Occlus-ion for 30 min followed by reperfusion 120 min. At the end of experiment, EEG, the tissue contents of sodium,potassium and water in the cerebral cortex, the activities of LDH and CPK in the cerebral venous blood and the maximal bleeding volume were estimated. Sanchinoside D1 ( 50mg/kg, i.v.) could ameliorate significantly all the changes of relevant parameters mentioned above in model animals. It was suggested that Sanchinoside D1 had some protective effect on acute cerebral ischemia in rabbits

The effect of anisodamine(654-2),aspirin(acetylsalicylic acid, ASA),prostacy-clin (PGI2)-like substance on whole blood platelet aggregation induced by adenosine diphos-phate ( ADP ) , arachidonic acid ( AA ) and ag-gregoserpentin of Trimersurus mucrosqumatus venom (TMVA) is reported, We found that ADP,AA and TMVA caused a dose-related increase in whole blood platelet aggregation, and the impedance technique was a sensitive method to evaluate the response of platelet in physiological condition. 654-2 could promote whole bloodplatelet aggregation induced by ADP, while ASAor PGI2-like substance could obviously inhibit the whole blood platelet aggregation induced by ADF or AA, but they failed to prevent TMVA-induced aggregation, suggesting that TMVA might mediate third pathway of platelet aggregation similar to platelet activiting faetor(PAF). Furthermore, the platelet stimulated by ADP or AA was still activated by TMVA, the mechanism of which remains to be studied.

After 45 min ligation of the gerbils' bilateral carotid arteries and then 24h reperfusion,the effects of water soluble Pollen flavone element from buckwheat, Isocorydine on the stroke index of 45 min cerebral ischemia followed by reperfusion 6h and the mortality of reperfusion 24h were evaluated .The results indicated that pollen element from buckwheat could decrease the stroke index and mortality rate dramatically, while Isocorydine had no effects.It was speculated that the beneficial effects of pollen element from buckwheat on cerebral damage following ischemia with reperfusion might be due to its depressing effect on the metabolism of free radicals.