Thromb Haemost 1975; 34(01): 050-062
DOI: 10.1055/s-0038-1651445
Original Article
Schattauer GmbH

The Influence of Ascorbic Acid on Platelet Structure and Function

Dale H Cowan
1   Department of Medicine, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital and University Hospitals, Cleveland, Ohio, U.S.A.
,
Richard C Graham Jr.
1   Department of Medicine, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital and University Hospitals, Cleveland, Ohio, U.S.A.
,
Patricia Shook
1   Department of Medicine, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital and University Hospitals, Cleveland, Ohio, U.S.A.
,
Ronda Griffin
1   Department of Medicine, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital and University Hospitals, Cleveland, Ohio, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 03 September 1974

Accepted 04 May 1975

Publication Date:
02 July 2018 (online)

Summary

To determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidifìcation levels. The effect of ascorbic acid (A. A.) was compared to that of HCl and citric acid (C. A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A. A. and C. A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultra-structure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A. A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

 
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