Effect of pulse polarity and energy on ultrasound-induced lung hemorrhage in adult rats.

Abstract

The objective of this study was to further assess the role of inertial cavitation in ultrasound-induced lung hemorrhage by examining the effect of pulse polarity at a common in situ (at the lung surface) peak rarefactional pressure [pr(in situ)] and at a common in situ pulse intensity integral (PII(in situ)). A total of 60 rats was divided into three experimental groups of 20 animals per group and randomly exposed to pulsed ultrasound. The groups were exposed as follows: Group 1 to 0 degree polarity pulses (compression followed by rarefraction) at a pr(in situ) of 3.48 MPa and a PII(in situ) of 4.78 Ws/m2, group 2 to 180 degree polarity pulses (rarefraction followed by compression) at a pr(in situ) of 3.72 MPa and a PII(in situ) of 2.55 Ws/m2, and group 3 to 180 degree polarity pulses at a pr(in situ) of 4.97 MPa and a PII(in situ) of 4.79 Ws/m2. For all experimental groups, the frequency was 2.46 MHz, the exposure duration was 240 s, the pulse repetition frequency was 2.5 kHz, and the pulse duration was 0.42 micros. Six sham animals were also randomly distributed among the experimental animals. The lesion surface area and depth were determined for each rat as well as lesion occurrence (percentage of rats with lesions) per group. It was found that lesion occurrence and size correlated better with PII(in situ) than with pr(in situ), suggesting that a mechanism other than inertial cavitation was responsible for the damage.