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Thromb Haemost 1980; 44(02): 065-068
DOI: 10.1055/s-0038-1650085
Original Article
Schattauer GmbH Stuttgart

Kinetics and in Vivo Redistribution of 111Indium-Labelled Human Platelets after Intravenous Protamine Sulphate

A duP Heyns
(*)   The Department of Haematology, University of the Orange Free State, Bloemfontein, South Africa
,
M G Lötter
(**)   The Department of Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
P N Badenhorst
(*)   The Department of Haematology, University of the Orange Free State, Bloemfontein, South Africa
,
H Kotze
(*)   The Department of Haematology, University of the Orange Free State, Bloemfontein, South Africa
,
F C Killian
(*)   The Department of Haematology, University of the Orange Free State, Bloemfontein, South Africa
,
C Herbst
(**)   The Department of Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
O R van Reenen
(**)   The Department of Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
P C Minnaar
(**)   The Department of Biophysics, University of the Orange Free State, Bloemfontein, South Africa
› Author Affiliations
Further Information

Publication History

Received 11 April 1980

Accepted 04 August 1980

Publication Date:
13 July 2018 (online)

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Summary

The pathogenesis of thrombocytopenia induced by intravenous protamine sulphate was studied in six patients who underwent cardiopulmonary bypass surgery, and in three normal volunteers. Autologous platelets were labelled with 111Indium-oxine. Platelet lifespan was determined. In vivo 111In-platelet localization, organ redistribution and sites of destruction were quantitated with a scintillation camera and a computer-assisted imaging system. Protamine induced a transient thrombocytopenia, maximal 5-10 min after injection, and 30-40 min in duration. The thrombocytopenia was accompanied by a transient accumulation of platelets in the liver. The splenic platelet pool remained unaltered and no platelets accumulated in the lungs. Platelet survival, measured in two volunteers, was slightly longer than normal and fitted a linear function best. There was a severe transient neutropenia during the period of thrombocytopenia. We conclude that protamineinduced thrombocytopenia is caused by hepatic accumulation of "activated" platelets or platelet aggregates, the process is reversible, and in the two normal volunteers studied, platelet survival was not affected.

Key words

Platelet kinetics - 111Indium-oxine labelled human platelets - Protamine sulphate - Thrombocytopenia, protamine induced - Neutropenia, protamine induced
 

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