Abstract:

It has been shown that application of cw ultrasound at 1--8-W/cm2 SATA intensities and megahertz frequencies can accelerate the dissolution of blood clots when a clot-lysing agent is present. To determine whether or not a cavitational mechanism is responsible for ultrasound accelerated thrombolysis (UAT), a hyperbaric chamber was constructed that can apply 10 atm of static air overpressure to an in vitro exposure apparatus. Five hundred (mu) fibrin clots overlaid with a clot-lysing agent were exposed to 4-W/cm2 SATA ultrasound at 1 MHz and lysis quantified via release of bound radiolabel as a function of overpressure. More than half the acceleration due to ultrasound was removed, suggesting a bubble mechanism is responsible at least in part for UAT. Transmission and reflection of 20-MHz tone bursts of 0.5 (mu) duration provide evidence that bubble activity was reduced concomitantly during overpressure. [Work supported by NIH.]