Can therapeutic ultrasound damage human platelets in vivo?

Abstract

It has recently been shown that therapeutic intensities of ultrasound decreased the recalcification time of anticoagulated whole blood in vitro. Further studies suggested that the megahertz ultrasound interacted with the blood platelets (i.e., the exceptionally fragile cells which participate in the early stages of clot formation) possibly via the occurrence of some form of cavitationlike activity. Subsequent in vitro work has demonstrated that therapeutic ultrasound can also induce platelet aggregation and the release of the platelet‐specific protein, β‐thromboglobulin (β‐TG), confirming that the platelet is the probable site of interaction and damage. Acoustic microstreaming similar to that developed around oscillating gas bubbles has been shown to produce platelet thrombi and true clots within the intact vascular system of mice in vivo. Similarly, irradiation of the blood supply to the pinnae of anaesthetized guinea pigs with therapeutic ultrasound has resulted in the entrapment of platelet microemboli within the intact capillary bed. Consequently, a series of experiments have been undertaken to see if therapeutic ultrasound can disrupt or otherwise induce human platelets to undergo the release reaction during irradiation in vivo. A butterfly cannula was inserted into the median cubital vein of young adult volunteers and three sequential blood samples taken into iced EDTA/theophylline. The blood collected as the second sample, was irradiated with 0.75‐MHz ultrasound (spatially averaged intensity 0.34–0.5 W cm−2, continuous wave) while still without the vein. No significant elevation of β‐TG was observed in the sonicated samples, however, this may be a reflection of the collection procedure which did not allow enough time for the platelet aggregation‐release‐aggregation cycle to become established.