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Clinical and Research Facilities, Centrallslip State Hospital, and Nassau County Hospital for Pulmonary Diseases, PlainviewIn a previous studyl an attempt was made tD evaluate the antianxiety effects of chlDrmezanone alone and in cDmbinatiDn with aspirin. The results suggested clinical activity which we felt warranted further study in terms Df determining cDmparative efficacy with a standard, widely accepted therapeutic agent. The present study considers the clinical effect of chlormezanDne and meprobamate in a double-blind placebD cDntrolled comparative trial. MethodSixty-seven patients, 41 WDmen (20 tD 77 years DId) and 26 men (18 to 60 years DId) were assigned at randDm to chlormezanDne, meprDbamate, Dr placebD ther-

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We have examined the possibility that substances released during platelet degranulation modify vascular PGI2 synthesis. PGI2 is a potent inhibitor of platelet function produced by vascular endothelial and smooth muscle cells. Regulation of PGI2 synthesis by blood vessels is not well understood. We report that a platelet- dependent factor in serum dramatically stimulates PGI2 synthesis by vascular endothelial and smooth muscle cells in culture. We further report that platelet-derived growth factor (PDGF), a releasable protein found in platelet alpha granules, stimulates PGI2 synthesis by the above cell types by over 100 fold. The concentration of PDGF required to elicit this effect is below that reported in human serum. The above mentioned serum factor is relatively heat stable, non-dialyzable, and cationic; preliminary studies indicate that anti-PDGF antiserum is capable of blocking stimulation of PGI2 synthesis by both PDGF and serum. These data suggest that the serum factor may indeed be PDGF. PDGF acts synergistically with other platelet granule constituents (serotonin, ATP) and with thrombin to stimulate PGI2 synthesis by vascular cells in culture. We thus postulate that platelet-released PDGF, in concert with other substances generated during clotting, acts to increase vessel wall PGI2 synthesis as part of a negative feedback mechanism controlling platelet aggregation. A defect in the ability of a blood vessel to increase PGI2 production in response to platelet degranulation, as may occur in atherosclerotic vessels, could perhaps contribute to the genesis of thromboembolic events.