This paper is to report our study on the effects of indomethacin, fenbufen, ksto profen, naproxen and doxamethasone on the number of leucocytes, the phagocytosis of macrophages and the intracellucar cAMP level in the peptone induced peritoneal exudate of mouse and on the comparison of thses drugs with dexametha-sone.Under therapeutic dosage, indomethacin and ketoprofen could significantly decrease the number of leucocytes in the exudate (P

Twenty four hours after occluding of the middle cerebral artery in rats, thecirculating neutrophils were in activated state and the lipidperoxidation increased in ische-mic brain tissue. Tanshinone inhibited the chemoluminescence of the circulating neutrophilphagocytosis and decreased leukocyte infiltration in infarcted brain tissue. It alsodecreased lipoperoxide, malondialdehyde and increased SOD activity in ischemic cerebralregion. In addition, it reduced cerebral infarction size in the model. The correlationbetween inhibitory effects on leukocyte and reduction in ischemic cerebral damage wassignificant. Dexamethasone used as a positive control had similar effects on neutrophils andischemic cerebral injury. It was shown that the prophylactic effcts of Tanshinone oncerebral infarction might be mainly due to its inhibition on leukocyte function.

It was found that there was a significant increase of the number of circulating leucocytes 2h after a subcutaneous injcetion of isoprenaline and severe myocardial necrosis occurred after consecutive injections for 3 d.Cytoxan-induced depletion of leucocytes resulted in an obvious decrease of the percentage of myocardial necrosis.In the control.the neutrophilic phagocytosis was enhanced and their release of acid phosphatase elevated greatly,which indicates that the neutrophils are in an activated state.After the.neutrophils were inhibited with dexamethasone or indomethacint significant reduction of the contents of prostaglandin E2 and malondialdehyde and an increase of superoxide dismutase activty in the myocardium were observed and consequently myocardial necrosis was greatly alleviated.Our findings suggest that neutrophils might play an important role in the pathogenesis of myocardial infarction through the release of lysosomal enzymes and the production of oxygen-derived free radicals and certain metabolites of arachidonic acid,and proper regulation of the neutrophilic functions could exert prophylactic effects on myocardial infarction.This might be a promising direction to look for more effective drugs to treat myocardial infarction.

The relationship between the inhibitory effect of tetrandrine ( Tet ) on neutrophil ( Nen ) lysomal enzyme ( ?-glu-curonidasc , P-G ) release & calcium ion were studied. It was found that calcium ion added to the medium increased p-G release from Neu During incubation. After intracellular calcium was depleted by EGTA, P-G release was signifcantly decreased. While calcium was added, increase in P-G release reappeared. It indicated that both intracellular & extracellular calcium may be involved in P-G release. Tet & v erapamil ( Ver ) not only inhibited ?-G release induced either by calcium or serum opsonized zymOsan, but also inhibited potential operated channel of Neu. It was concludted that the inhibitory effect of Tet on Neu lysomal enzyme release was concerned with its calcium antagonism.