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Biomedical subjects

M B Zucker

Publications and source records attributed to M B Zucker.

At least 73 records · Page 4Linked to original sources
PubMed1975

Procoagulant activity of platelets in recalcified plasma.

High-spun platelet-poor plasma (HSPPP) and platelet-rich plasma (PRP), prepared with minimal contact activation and pH shifts, were recalcified with little dilution in the presence of phospholipid prepared from chloroform-extracted, acetone-dried brain tissue. The clotting times of HSPPP and PRP were the same whether or not the platelets in PRP were first incubated or aggregated with ADP or with collagen. This suggests that platelet procoagulant activity in normal recalcified plasma derives only from provision of platelet phospholipid.

Blood Coagulation Tests↗
PubMed1974

The tumor-promoter phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate), a potent aggregating agent for blood platelets.

The phorbol ester 12-0-tetradecanoyl-phorbol-13-acetate, a potent tumor-promoting agent, caused irreversible platelet aggregation when more than 0.02 microM was stirred with human citrated or heparinized platelet-rich plasma (PRP). With washed platelets, 1 nM was effective. The alcohol phorbol, which has little tumor-promoting activity, failed to cause platelet aggregation. With all but low concentrations of phorbol ester, aggregation was succeeded by a rapid phase. The latter was prevented or reduced by enzymes which destroy ADP and by aspirin, was associated with a change in platelet shape, and was presumably due to released ADP. At higher concentrations, only a rapid phase was seen, and these inhibitors were not effective. Low concentrations did not aggregate platelets in PRP containing sufficient EDTA or EGTA to chelate ionized calcium or in PRP from thrombasthenic patients; higher concentrations caused slight aggregation. Both the primary, non-ADP-dependent aggregation and the rapid ADP-dependent aggregation were markedly inhibited by substances which increase cyclic AMP, metabolic inhibitors, and the sulfhydryl inhibitor N-ethylmaleimide. Phorbol ester reduced platelet cyclic AMP only when it had been previously elevated by prostaglandin E(1). 1 microM did not release beta-glucuronidase, lactic dehydrogenase, or inflammatory material from platelets in 4-5 min despite marked aggregation, but liberated all three in 30 min. The possibility is discussed that low phorbol ester concentrations cause primary aggregation by a direct action on platelet actomyosin.

Adenosine Diphosphate↗