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

Marjorie B. Zucker

doi:10.1055/s-0038-1649023

Thrombosis and Haemostasis, Inhaltsverzeichnis

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

¹Department of Pathology, New York University School of Medicine, New York, N. Y. 10016

› Institutsangaben

Abstract

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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