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Thromb Haemost 1976; 36(01): 221-229
DOI: 10.1055/s-0038-1648027
Original Article
Schattauer GmbH

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function[*]

Charles A. Schiffer
1   Clinical Oncology Branch and the Laboratory of Pharmacology, National Cancer Institute, Baltimore Cancer Research Center, 22 South Greene Street, Baltimore, Maryland, 21201
2   Baltimore Rh Typing Laboratory, 513 West Lombard Street, Baltimore, Maryland, 21201.
,
Caroline L. Whitaker
1   Clinical Oncology Branch and the Laboratory of Pharmacology, National Cancer Institute, Baltimore Cancer Research Center, 22 South Greene Street, Baltimore, Maryland, 21201
2   Baltimore Rh Typing Laboratory, 513 West Lombard Street, Baltimore, Maryland, 21201.
,
Morton Schmukler
1   Clinical Oncology Branch and the Laboratory of Pharmacology, National Cancer Institute, Baltimore Cancer Research Center, 22 South Greene Street, Baltimore, Maryland, 21201
2   Baltimore Rh Typing Laboratory, 513 West Lombard Street, Baltimore, Maryland, 21201.
,
Joseph Aisner
1   Clinical Oncology Branch and the Laboratory of Pharmacology, National Cancer Institute, Baltimore Cancer Research Center, 22 South Greene Street, Baltimore, Maryland, 21201
2   Baltimore Rh Typing Laboratory, 513 West Lombard Street, Baltimore, Maryland, 21201.
,
Steven L. Hilbert
1   Clinical Oncology Branch and the Laboratory of Pharmacology, National Cancer Institute, Baltimore Cancer Research Center, 22 South Greene Street, Baltimore, Maryland, 21201
2   Baltimore Rh Typing Laboratory, 513 West Lombard Street, Baltimore, Maryland, 21201.
› Author Affiliations
Further Information

Publication History

Received 23 February 1976

Accepted 08 April 1976

Publication Date:
03 July 2018 (online)

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Summary

Although dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

* Presented in part at the Annual Meeting of the American Association of Blood Banks, November, 1975.


 

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