Volume 9, Issue 4 pp. 145-151
Original Article
Full Access

The use of β-Thromboglobulin to detect platelet damage by therapeutic ultrasound in vivo

Alun R. Williams phD

Corresponding Author

Alun R. Williams phD

Department of Medical Biophysics, University of Manchester Medical School, Manchester

ICI Central Toxicology Laboratory, Cheshire

Medical Products Development Department, The Radiochemical Centre, Amersham, Buckinghamshire, England

The Department of Medical Biophysics, University of Manchester Medical School, Stopford Building, Oxford Road, Manchester, EnglandSearch for more papers by this author
Bernard V. Chater phD

Bernard V. Chater phD

Department of Medical Biophysics, University of Manchester Medical School, Manchester

ICI Central Toxicology Laboratory, Cheshire

Medical Products Development Department, The Radiochemical Centre, Amersham, Buckinghamshire, England

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Kenneth A. Allen BSc

Kenneth A. Allen BSc

Department of Medical Biophysics, University of Manchester Medical School, Manchester

ICI Central Toxicology Laboratory, Cheshire

Medical Products Development Department, The Radiochemical Centre, Amersham, Buckinghamshire, England

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Joel H. Sanderson MB, ChB

Joel H. Sanderson MB, ChB

Department of Medical Biophysics, University of Manchester Medical School, Manchester

ICI Central Toxicology Laboratory, Cheshire

Medical Products Development Department, The Radiochemical Centre, Amersham, Buckinghamshire, England

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First published: April 1981
Citations: 8

Abstract

Three sequential blood samples were drawn from arms of adult human volunteers by means of a cannula technique, and the plasma levels of β-thromboglobulin (β-TG, an index of platelet damage) were measured. Ultrasound (0.75 MHz, continuous wave; spatially averaged intensity 0.34 to 0.5 W/cm–2) was applied to the blood vessels while the second sample of each series was being taken. No elevation of β-TG was detected, indicating that under these conditions ultrasonic irradiation had not damaged an appreciable number of platelets. There was, however, an indication of decreased platelet sensitivity following insonation; and it is postulated that this may be the result of either increased production or secretion of the potent endothelial platelet inhibitor, prostacyclin, or both.

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