Hepatic lesions in the rabbit induced by acoustic cavitation

Prat, Frédéric; Ponchon, T.; Berger, F.; Chapelon, J.Y.; Gagnon, P.; Cathignol, D.

doi:10.1016/0016-5085(91)90788-m

Cited by 19 publications

(7 citation statements)

References 23 publications

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“…This observation led to the design of experiment 3 where the influence of gas bubbles was systematically examined. In retrospect, the setup corresponded to the one published by Prat et al (1992) who found in an in vivo study a dramatic increase in tissue damage in rabbit livers when gas bubbles were injected during shock wave application.…”

Section: Discussionmentioning

confidence: 81%

“…There is evidence that the interaction between a shock wave and gas bubbles is a crucial event for the formation of tissue damage. Tissue damage was increased when the interaction was facilitated by a fast shock wave administration rate (Delius et al, 1990a,b) and also when small gas bubbles of micrometer size were injected into the hepatic artery during shock wave administration to the liver (Prat et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

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Extracorporeal shock waves stimulate frog sciatic nerves indirectly via a cavitation-mediated mechanism

Schelling

Delius

Gschwender

et al. 1994

Biophysical Journal

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Shock waves (SWs) are single pressure pulses with amplitudes up to over 100 MPa, a rise time of only a few nanoseconds, and a short duration of approximately 2 microseconds. Their clinical application for stone destruction causes pain, indicating nerve stimulation by SWs. To examine this phenomenon, sciatic nerves of frogs were exposed to SWs in an organ bath. The SWs were generated with an experimental Dornier lithotripter model XL1 at an operating voltage of 15 kV. The nerves were mounted in a chamber which allowed electrical nerve stimulation and the registration of electrically and SW-induced compound action potentials (SWCAPs). The chamber was filled with frog Ringer's solution. In a standardized protocol. The first experiment established that 95.0 +/- 4.7% of administered SWs induced action potentials which were lower in amplitude (1.45 +/- 1.14 versus 1.95 +/- 0.95 mV, p = 0.004) but similar in shape to electrically induced compound action potentials. In a second experiment, it was shown that the site of origin of the SWCAPs could be correctly determined by simultaneous recording of action potentials at both ends of the nerve. The mechanism of shock wave stimulation was examined by experiments 3 and 4. In experiment 3, in contrast to the previous experiments, SW exposure of the nerves was performed 6 cm outside the shock wave focus. This resulted in a mean probability of inducing a SWCAP of only 4%. After gas bubble administration, this probability increased to 86% for the first SW released immediately after bubble application and declined to 56% for the second, 21% for the third, to 0 for the 10th SW after fluid injection. This indicates that cavitation, the interaction between shock waves and gas bubbles in fluid or tissues, was involved in SWCAP generation. In experiment 4, nerves were again exposed in the focus, however, the Ringer's solution surrounding the nerve was replaced by polyvinyl alcohol (PVA). PVA is a solution with low cavitation activity.In PVA, the excitability was markedly diminished to 11.0 +/- 5.1% compared with 96.0 +/- 4.4% in control nerves exposed in Ringer's solution. In conclusion, bioeffects of SWs on nervous tissue appear to result from cavitation. It is suggested that cavitation is also the underlying mechanism of SW-related pain during extracorporeal SW lithotripsy in clinical medicine.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Extracorporeal shock waves stimulate frog sciatic nerves indirectly via a cavitation-mediated mechanism

Schelling

Delius

Gschwender

et al. 1994

Biophysical Journal

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“…Tissue studies using ultrasound shock waves also support cavitation induced damage, e.g. hemorrhage and cellular membrane poration [26][27][28] . In addition, cavitation in blood vessels has been shown to result in air emboli that can reach the brain causing cerebral infarct 29,30 .…”

Section: Such Cavitation Damage Of Materials Surfaces Is Well Establismentioning

confidence: 96%

Localized Tissue Surrogate Deformation due to Controlled Single Bubble Cavitation

Yang¹,

Sarntinoranont²,

Canchi³

et al. 2014

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Cavitation-induced shock wave, as might occur in the head during exposure to blast waves, was investigated as a possible damage mechanism for soft brain tissues. A novel experimental scheme was developed to visualize and control single bubble cavitation and its collapse, and the influence of this process on a nearby tissue surrogate was investigated. The experiment utilized a Hopkinson pressure bar system which transmits a simulated blast pressure wave (with over and under pressure components) to a fluid-filled test chamber implanted with a seed gas bubble. Growth and collapse of this bubble was visually recorded during passage of the blast wave with a high speed

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“…15 Another important mechanism of tissue damage is the piercing effect of a liquid microjet with an impact velocity of more than 200 m/s, which is formed through the interaction of a tiny bubble and a shock wave. [15][16][17][18][19] Once hemorrhage had occurred in our patient, the weight of the blood clot cut the vessel between the liver parenchyma and the capsule. Thus, the hematoma increased.…”

Section: Discussionmentioning

confidence: 98%

Hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for pancreatic stones

Hirata

Kushida

Ohguri

et al. 1999

Journal of Gastroenterology

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We present a patient with complication of huge hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for pancreatic lithotripsy. The hematoma measured 78-110mm. Angiography showed a subcapsular hematoma, rather than a hematoma in the liver. In the arterial phase, the distal end of the small vessel showed spotty opacification similar to microaneurysma, suggesting that it was an injury caused by separation of the liver and its capsule, caused by the shock waves. The portal vein and hepatic vein were normal. After 8 weeks of conservative therapy, the hematoma was gradually absorbed and the patient was discharged. Eight months after the accident, the hematoma had decreased to 40mm in size. After 20 months, it was completely absorbed. The reported rate of renal subcapsular hematoma after ESWL for renal or ureter stones is 0.1%-0.7%. To date, however, only five cases of hepatic subcapsular hematoma after right renal stone disintegration have been reported. This is the first report of hepatic subcapsular hematoma after ESWL for pancreatic stones.

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Hepatic lesions in the rabbit induced by acoustic cavitation

Cited by 19 publications

References 23 publications

Extracorporeal shock waves stimulate frog sciatic nerves indirectly via a cavitation-mediated mechanism

Extracorporeal shock waves stimulate frog sciatic nerves indirectly via a cavitation-mediated mechanism

Localized Tissue Surrogate Deformation due to Controlled Single Bubble Cavitation

Hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for pancreatic stones

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