Thromb Haemost 1980; 44(02): 100-104
DOI: 10.1055/s-0038-1650093
Original Article
Schattauer GmbH Stuttgart

Kinetics and Fate of 111Indium-Oxine Labelled Blood Platelets in Asplenic Subjects

Anthon duP Heyns
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
Matthys G Lötter
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
Philip N Badenhorst
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
Otto van Reenen
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
Henry Pieters
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
,
Phil C Minnaar
Departments of Haematology and Biophysics, University of the Orange Free State, Bloemfontein, South Africa
› Author Affiliations
Further Information

Publication History

Received 24 March 1980

Accepted 29 August 1980

Publication Date:
13 July 2018 (online)

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Summary

The survival, tissue distribution and fate of 111Indium-oxine labelled autologous platelets was studied in four asplenic subjects with serial blood sampling, scintillation camera and computer-assisted imaging. Mean 111In-platelet recovery in the circulation was 89 ± 13% (± 1 SD). Platelet survival curves fitted a linear function best and was 238 ± 41 h. The shape of the survival curves of normal and asplenic subjects differed: in the asplenic subjects the curve was linear whereas that of normal subjects was significantly more curvilinear if analyzed by least squares computer fitting to a gamma function. Early hepatic 111In-activity was significant and transient and ascribed to the "collection injury". As labelled platelets disappeared from the circulation, 111Inactivity in the liver increased progressively and linearly to reach 42.5 ± 14.1 % of whole body activity at 240 h. Radioactivity also accumulated in the bone marrow, but could not be demonstrated in the vasculature of the lower limbs. These results would indicate that in asplenic subjects the major sites of destruction of senescent platelets are the liver and bone marrow.