Acoustically induced shear stresses in the vicinity of microbubbles in tissue

Lewin, Peter A.; Björnö, L.

doi:10.1121/1.387549

Cited by 59 publications

(38 citation statements)

References 13 publications

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“…Inertial (or transient) cavitation bubbles grow faster, expanding two to three times their resonant size, where they oscillate unstably, and finally collapse in a single compression half-cycle [84]. Although it has been proposed that damage to biological tissues can theoretically occur from stable cavitation bubbles [85], it is generally accepted that the primary mechanism for structurally altering intact cells is inertial cavitation, where these alterations include both irreversible damage [86] as well as non-destructive increases in membrane permeability [87].…”

Section: Acoustic Cavitationmentioning

confidence: 99%

Ultrasound mediated delivery of drugs and genes to solid tumors

Frenkel

2008

Advanced Drug Delivery Reviews

426

334

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It has long been shown that therapeutic ultrasound can be used effectively to ablate solid tumors, and a variety of cancers are presently being treated in the clinic using these types of ultrasound exposures. There is, however, an ever-increasing body of preclinical literature that demonstrates how ultrasound energy can also be used non-destructively for increasing the efficacy of drugs and genes for improving cancer treatment. In this review, a summary of the most important ultrasound mechanisms will be given with a detailed description of how each one can be employed for a variety of applications. This includes the manner by which acoustic energy deposition can be used to create changes in tissue permeability for enhancing the delivery of conventional agents, as well as for deploying and activating drugs and genes via specially tailored vehicles and formulations.

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Section: Acoustic Cavitationmentioning

confidence: 99%

Ultrasound mediated delivery of drugs and genes to solid tumors

Frenkel

2008

Advanced Drug Delivery Reviews

426

334

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“…Examples such as these represent a common notion that cavitation bioeffects are induced in the US field by microbubbles in the liquid medium external to a cell surface-whether they are in the medium above the cell culture or in the lumen of a blood vessel near the endothelium-and that the microbubbles apply mechanical stress on the surface (see, e.g., refs. [16][17][18]. The amplification of the pressure amplitude by a nearby microbubble is studied in a third model (model III) for a bubble in proximity to a solid boundary.…”

mentioning

confidence: 99%

Intramembrane cavitation as a unifying mechanism for ultrasound-induced bioeffects

Krasovitski

Frenkel

Shoham

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

449

375

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The purpose of this study was to develop a unified model capable of explaining the mechanisms of interaction of ultrasound and biological tissue at both the diagnostic nonthermal, noncavitational (<100 mW·cm −2) and therapeutic, potentially cavitational (>100 mW·cm −2 ) spatial peak temporal average intensity levels. The cellular-level model (termed "bilayer sonophore") combines the physics of bubble dynamics with cell biomechanics to determine the dynamic behavior of the two lipid bilayer membrane leaflets. The existence of such a unified model could potentially pave the way to a number of controlled ultrasound-assisted applications, including CNS modulation and blood-brain barrier permeabilization. The model predicts that the cellular membrane is intrinsically capable of absorbing mechanical energy from the ultrasound field and transforming it into expansions and contractions of the intramembrane space. It further predicts that the maximum area strain is proportional to the acoustic pressure amplitude and inversely proportional to the square root of the frequency (ε A;max ∝ P 0:8 A f − 0:5 ) and is intensified by proximity to free surfaces, the presence of nearby microbubbles in free medium, and the flexibility of the surrounding tissue. Model predictions were experimentally supported using transmission electron microscopy (TEM) of multilayered live-cell goldfish epidermis exposed in vivo to continuous wave (CW) ultrasound at cavitational (1 MHz) and noncavitational (3 MHz) conditions. Our results support the hypothesis that ultrasonically induced bilayer membrane motion, which does not require preexistence of air voids in the tissue, may account for a variety of bioeffects and could elucidate mechanisms of ultrasound interaction with biological tissue that are currently not fully understood.A central hypothesis regarding nonthermal interactions of ultrasound (US) energy and biological tissue is that they are primarily mediated by cavitation, that is, the activity in the US field of gas bubbles generated from submicron-sized gas pockets known as cavitation nuclei: their steady pulsations (stable cavitation) or rapid collapse (inertial cavitation) (1) and their interaction with cells, tissue, and organs (2-4). Nevertheless, this hypothesis has major limitations because low-intensity noncavitational US exposures of <100 mW·cm −2 , spatial peak temporal average (SPTA), have also been shown to induce bioeffects in cells and tissues without evidence of inertial or stable cavitation being present (3-5). On the other hand, whereas the source of in vivo cavitation is not clear, the bilayer membrane seems to be associated with many of the cellular bioeffects at a wide range of US intensities: from excitation of neuronal circuits [3 W·cm −2 spatial peak temporal peak (SPTP), 0.44 MHz] (6) to increased transfection rates in smooth muscle cells (400 mW·cm −2 SPTP, 1 MHz) (7). Our objective here is to introduce a unique hypothesis of direct interaction between the oscillating acoustic pressure and the cellular bilayer memb...

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“…(5.9). The shear stress resulting from microstreaming near a pulsating bubble resting on cell membrane (Lewin and Bjørnø 1982) and near a living cell (Wu 2002) can be numerically estimated by considering the cell to be a solid boundary.…”

Section: Shear Stress Induced By Microstreamingmentioning

confidence: 99%