Vessel damage mechanisms by ultrasound or shock wave pulses

Abstract

Edwin L. Carstensen has been one of the pioneers investigating not only the thresholds for bioeffects of ultrasound, but also determining mechanisms for these bioeffects, especially when air cavities are involved. Previous studies have demonstrated that hemorrhage or endothelial layer damage can occur when the blood vessels are exposed to lithotripter shock waves or to ultrasound in the presence of echo contrast agents. The presence of bubbles is often necessary for the damage to occur. Two main hypotheses describing the mechanism of vessel damage by acoustically excited microbubbles have been proposed. The vessel could be damaged by the high pressures and/or temperatures generated by the violent collapse of cavitation bubbles. Alternatively, the vessel could rupture upon bubble expansion. Here, a simple model is presented for vessel rupture upon bubble expansion and calculations are presented for parameters corresponding to two recently published experimental observations of vessel rupture and of endothelial cell damage to try to distinguish between these two mechanisms.