Release of beta-thromboglobulin from human platelets by therapeutic intensities of ultrasound

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 was increased and also as the driving frequency was decreased from 3.0 to 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 in the presence of inhibitors which rendered the platelets functionally inert. Our data suggests that beta-TG is liberated in two ways, firstly 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.