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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Weiss, H. Articles by Turitto, V. Search for Related Content PubMed PubMed Citation Articles by Weiss, H. Articles by Turitto, V. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Correction of the platelet adhesion defect in delta-storage pool deficiency at elevated hematocrit--possible role of adenosine diphosphate HJ Weiss, B Lages, T Hoffmann and VT Turitto Department of Medicine, St. Luke's-Roosevelt Hospital Center, New York, NY 10019, USA. Previous studies on patients with storage pool deficiency (SPD) who are specifically deficient in platelet dense granules (delta-SPD) have suggested a role for dense granule substances, in all likelihood adenosine diphosphate (ADP), in mediating thrombus formation on subendothelium at high shear rates. The role of dense granule substances in mediating platelet adhesion appears to be more complicated Previous studies in delta-SPD suggested an adhesion defect that was strongly influenced by the patient's hematocrit (Hct) value. To explore further the possibility that red blood cells (RBCs) may influence the role that platelet storage granules play in mediating adhesion at high shear rates, we have measured adhesion (and thrombus formation) throughout a preselected range of Hct values (30% to 60%) in normal subjects and in patients with delta-SPD. The present studies confirm the defect in platelet adhesion in patients with delta-SPD, most significantly at Hct values of 30% to 40%. This defect (but not that of thrombus formation) can be completely corrected by the addition of RBCs. The correction of the platelet adhesion defect by RBCs was specific for delta-SPD; it was not observed in either von Willebrand's disease or thrombasthenia. Studies performed on normal blood under conditions that could be expected to block any effect of ADP on adhesion and an analysis of the type of adhesion defect in delta-SPD suggest that ADP may be involved in the process required for platelet spreading on the subendothelium. The corrective effect of RBCs on platelet adhesion in delta-SPD appears to be chemical rather than physical in nature, possibly due to shear-induced release of RBC ADP or to other recently described properties of RBCs that enhance collagen- induced platelet interactions. Volume 87, Issue 10, pp. 4214-4222, 05/15/1996 Copyright © 1996 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. J. Hathcock Flow Effects on Coagulation and Thrombosis Arterioscler Thromb Vasc Biol, August 1, 2006; 26(8): 1729 - 1737. [Abstract] [Full Text] [PDF] K. Suzuki-Inoue, Y. Yatomi, N. Asazuma, M. Kainoh, T. Tanaka, K. Satoh, and Y. Ozaki Rac, a small guanosine triphosphate-binding protein, and p21-activated kinase are activated during platelet spreading on collagen-coated surfaces: roles of integrin alpha 2beta 1 Blood, December 15, 2001; 98(13): 3708 - 3716. [Abstract] [Full Text] [PDF] D. Pratico, M. Pasin, O. P. Barry, A. Ghiselli, G. Sabatino, L. Iuliano, G. A. FitzGerald, and F. Violi Iron-Dependent Human Platelet Activation and Hydroxyl Radical Formation : Involvement of Protein Kinase C Circulation, June 22, 1999; 99(24): 3118 - 3124. [Abstract] [Full Text] [PDF]

	Copyright © 1996 by American Society of Hematology         Online ISSN: 1528-0020