Release of β-Thromboglobulin from Human Platelets by Therapeutic Intensities of Ultrasound

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Abstract
The effects of therapeutic intensities of ultrasound on human platelets in whole blood were investigated by monitoring the release of the platelet specific protein .beta.-thromboglobulin (.beta.-TG). More .beta.-TG was released as the intensity of the ultrasound increased and also as the driving frequency decreased from 3.0-0.75 mHz. Some .beta.-TG was released at spatially-averaged intensities as low as 0.6 W/cm2 at 0.75 mHz, a value significantly lower than that observed for the onset of aggregation of platelet rich plasma (obtained from the same volunteer) in the same exposure system. Liberation of .beta.-TG by ultrasound was diminished but not abolished with inhibitors which rendered the platelets functionally inert. .beta.-TG is apparently liberated in 2 ways: as a result of platelet disruption by cavitation, and subsequently by potent aggregating agents, liberated in parallel with .beta.-TG, inducing the physiological release reaction in adjacent platelets. The low therapeutic intensities and short exposure times (30 s or less) necessary to liberate .beta.-TG from normal human platelets in vitro, suggests that patients with abnormally sensitive platelets and/or hypercoagulable state could be at risk if subjected to high therapeutic intensities of ultrasound.
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