Thromb Haemost 1972; 28(03): 393-407
DOI: 10.1055/s-0038-1649023
Original Article
Schattauer GmbH

Proteolytic Inhibitors, Contact and Other Variables in the Release Reaction of Human Platelets

Marjorie B. Zucker
1   Department of Pathology, New York University School of Medicine, New York, N. Y. 10016
› Author Affiliations
Further Information

Publication History

Publication Date:
24 July 2018 (online)

Summary

Platelet-rich plasma (PRP) containing platelets labelled with 14C-serotonin was used to characterize the release reaction. Heparin promotes release, and the reduced release response to epinephrine observed in heparinized compared to citrated PRP is probably due to the earlier reaction. The release reaction can occur in citrated PRP at pH 7.0, is marked between pH 7.2 and 7.6, and decreases above pH 8.0. It is retained better when PRP is stored below pH 7.7. Adenosine, prostaglandin E1, and theophylline inhibit both aggregation and release, probably because they elevate cyclic AMP. D- and L-tosyl-phenylalanine chloromethylketone (TPCK) also inhibit both aggregation and release at a concentration of 0.1 mM whereas 0.1 mM D- and l-L-chloro-2-tosylamido-7-amino-2-heptanone (TLCK) and 5 mM diisopropylfluoro-phosphate (DFP), like aspirin, inhibit only release. Colchicine (0.1 mM) alters platelet shape but does not affect release or aggregation. Centrifugation of PRP at 37° C causes release which responds to inhibitors and pH changes in a manner similar to release induced by aggregation with ADP or epinephrine. Release occurs in thromb-asthenic platelets centrifuged at 37° C and is increased by epinephrine. Release of ATP and ADP correlates significantly with release of 14C-serotonin. Thrombin plus CaCl2 causes release of β-glucuronidase but not of zinc.

 
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