Abstract:The objective of this study was to assess the threshold and superthreshold behavior of ultrasound (US)-induced lung hemorrhage in adult rabbits to gain greater understanding about species dependency. A total of 99 76 ± 7.6-d-old 2.4 ± 0.14-kg New Zealand White rabbits were used. Exposure conditions were 5.6-MHz, 10-s exposure duration, 1-kHz PRF and 1.1-μs pulse duration. The in situ (at the pleural surface) peak rarefactional pressure, p r(in situ) , ranged between 1.5 and 8.4 MPa, with nine acoustic US expos… Show more
“…Thus, the mechanical mechanism(s) capable of causing such damage are likely related to the stress that focused ultrasound imposes directly on the lung's air-blood barrier such as radiation forces (Chu and Apfel 1982;Elrod et al 1989). We have shown that the histopathologic characteristics of the gross and microscopic lesions of pulsed ultrasound-induced lung hemorrhage are identical in four species (mice, rats, rabbits and pigs) (O'Brien et al 2006) and that hemorrhage in these species occurs at exposure conditions similar to those used for scanning in human beings. Thus, these findings suggested a common pathogenesis in the initiation and propagation of the lesions at the gross and microscopic levels; however, the exact mechanism of injury remained elusive.…”
Thermal injury, a potential mechanism of ultrasound-induced lung hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO 2 laser (wavelength ∼10.6 μm) was focused (680-μm beamwidth) on the surface of the lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 μm. After exposure, lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar hemorrhage. These results suggest that ultrasound-induced lung injury is most likely not caused by a thermal mechanism.
“…Thus, the mechanical mechanism(s) capable of causing such damage are likely related to the stress that focused ultrasound imposes directly on the lung's air-blood barrier such as radiation forces (Chu and Apfel 1982;Elrod et al 1989). We have shown that the histopathologic characteristics of the gross and microscopic lesions of pulsed ultrasound-induced lung hemorrhage are identical in four species (mice, rats, rabbits and pigs) (O'Brien et al 2006) and that hemorrhage in these species occurs at exposure conditions similar to those used for scanning in human beings. Thus, these findings suggested a common pathogenesis in the initiation and propagation of the lesions at the gross and microscopic levels; however, the exact mechanism of injury remained elusive.…”
Thermal injury, a potential mechanism of ultrasound-induced lung hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO 2 laser (wavelength ∼10.6 μm) was focused (680-μm beamwidth) on the surface of the lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 μm. After exposure, lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar hemorrhage. These results suggest that ultrasound-induced lung injury is most likely not caused by a thermal mechanism.
“…The variation in PCH observed with various limited parameter sets have been reviewed by AIUM (2000) and Church et al (2008). Different species have been used in the research, including mice, rats, rabbits, pigs, monkeys and humans (AIUM, 2000; O’Brien et al 2006; Church et al 2008). In addition, biological conditions are important, including age (Dalecki et al 1997; O’Brien et al 2003) and the specific anesthesia techniques (Miller et al 2014a; Miller et al 2015b).…”
The induction of pulmonary capillary hemorrhage (PCH) by pulsed ultrasound was discovered 25 yr ago but early research utilized fixed-beam systems rather than actual diagnostic ultrasound machines. In this study, fixed-beam focused ultrasound exposures for 5 min at 1.5 MHz and 7.5 MHz were performed in rats for comparison to recent research with diagnostic ultrasound. One exposure condition at each frequency used 10 µs pulses delivered at 25 ms intervals. Three conditions involved Gaussian modulation of the pulse amplitudes at 25 ms intervals to simulate diagnostic scanning: 7.5 MHz with 0.3 µs and 1.5 µs pulses at 100 µs and 500 µs pulse repetition periods, respectively, and 1.5 MHz with 1.7 µs pulses at 500 µs repetition periods. Four groups were tested for each condition to assess PCH areas at different exposure levels and to determine occurrence thresholds. The conditions with identical pulse timing showed smaller PCH areas for the smaller 7.5 MHz beam, but both had thresholds of 0.69–0.75 MPa in situ peak rarefactional pressure amplitude (PRPA). The Gaussian modulation conditions for 7.5 MHz with 0.3 µs pulses and 1.5 MHz with 1.7 µs pulses both had thresholds of 1.12–1.20 MPa PRPA, although the relatively long 1.5 µs pulses at 7.5 MHz gave a threshold of 0.75 MPa. The fixed-beam pulsed ultrasound exposures produced lower thresholds than diagnostic ultrasound. There was no clear tendency for thresholds to increase with increasing ultrasonic frequency when pulse timing conditions were similar.
“…[11] More importantly, the threshold of all UILH was within the range of diagnostic ultrasound and the mechanism of injury appeared to be specie and age independent; which increases the transposability of these findings to human fetuses. The possibility of a substantial temperature rise in the brain of fetuses when insonated in utero with diagnostic pulsed ultrasound have been demonstrated in guinea pigs, sheep, and human fetuses, [12] thus, again, demonstrating specie independent bioeffect.…”
Robust evidence of the bioeffects of ultrasound is available from animal studies but human studies are less convincing. Nevertheless, it is disturbing that the only response to safety issues is a twenty-year old principle known as ALARA (As Low As Reasonably Applicable). Using experience from obstetrics and toxicology, and drawing information mainly from two recent systematic reviews and meta-analysis that extensively covered the subject of ultrasound safety, this review captures the current knowledge of ultrasound bioeffects and suggests that it may be time for an international, multidisciplinary meeting on ultrasound safety to decide how to provide the evidence (available data) to patients and sonographers in a succinct manner.
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