Ultrasound-induced lung hemorrhage is not caused by inertial cavitation

In animal experiments, the pathogenesis of lung hemorrhage due to exposure to clinical diagnostic levels of ultrasound has been attributed to an inert ial cavitation mechanism. The purpose of this article is to report the resu lts of two experiments that directly contradict die hypothesis that ultraso und-induced lung hemorrhage is caused by inertial cavitation, Elevated hydr ostatic pressure was used to suppress the involvement of inertial cavitatio n. In experiment one, 160 adult mice were equally divided into two hydrosta tic pressure groups (0.1 or 1.1 MPa), and were randomly exposed to pulsed u ltrasound (2.8-MHz center frequency, 1-kHz PRF, 1.42-mu s pulse duration, 1 0-s exposure duration). For the two hydrostatic pressure groups (80 mice ea ch), 8 in situ peak rarefactional pressure levels were used that ranged bet ween 2.82 and 11.8 MPa (10 mice/group). No effect of hydrostatic pressure o n the probability of hemorrhage was observed. These data lend to the conclu sion that lung hemorrhage is not caused by inertial cavitation, Also, the h igher hydrostatic pressure enhanced rather than inhibited the impact of ult rasonic pressure on the severity (hemorrhage area, depth, and volume) of le sions. These counterintuitive findings were confirmed in a second experimen t using a 2 X 5 factorial design that consisted of two ultrasonic pressure levels and five hydrostatic pressure levels (100 mice, 10 mice/group). If i nertial cavitation were the mechanism responsible for lung hemorrhage, then elevated hydrostatic pressures should have resulted in less rather than mo re tissue damage at each ultrasonic pressure level. This further supports t he conclusion that the pathogenesis of ultrasound-induced lung hemorrhage i s not caused by inertial cavitation. (C) 2000 Acoustical Society of America . [S0001-4966(00)01309-6].