Bubble Motion in a Blood Vessel: Shear Stress Induced Endothelial Cell Injury

Mukundakrishnan, Karthik; Ayyaswamy, P. S.; Eckmann, David M.

doi:10.1115/1.3153310

Cited by 39 publications

(42 citation statements)

References 21 publications

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“…6–10 Findings from this work predict surfactant promotion of bubble detachment from the vessel wall through modification of its adhesion characteristics 11 . These results were confirmed in vivo with direct observation of accelerated embolism bubble clearance from the microcirculation of the rat cremaster muscle after administration of exogenous surfactant.…”

Section: Introductionmentioning

confidence: 83%

Mechanotransductional basis of endothelial cell response to intravascular bubbles

et al. 2011

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Vascular air embolism resulting from too rapid decompression is a well-known risk in deep-sea diving, aviation and space travel. It is also a common complication during surgery or other medical procedures when air or other endogenously administered gas is entrained in the circulation. Preventive and post-event treatment options are extremely limited for this dangerous condition, and none of them address the poorly understood pathophysiology of endothelial response to intravascular bubble presence. Using a novel apparatus allowing precise manipulation of microbubbles in real time fluorescence microscopy studies, we directly measure human umbilical vein endothelial cell responses to bubble contact. Strong intracellular calcium transients requiring extracellular calcium are observed upon cell-bubble interaction. The transient is eliminated both by the presence of the stretch activated channel inhibitor, gadolinium, and the transient receptor potential vanilliod family inhibitor, ruthenium red. No bubble induced calcium upsurge occurs if the cells are pretreated with an inhibitor of actin polymerization, cytochalasin-D. This study explores the biomechanical mechanisms at play in bubble interfacial interactions with endothelial surface layer (ESL) macromolecules, reassessing cell response after selective digestion of glycocalyx glycosoaminoglycans, hyaluran (HA) and heparin sulfate (HS). HA digestion causes reduction of cell-bubble adherence and a more rapid induction of calcium influx after contact. HS depletion significantly decreases calcium transient amplitudes, as does pharmacologically induced sydencan ectodomain shedding. The surfactant perfluorocarbon oxycyte abolishes any bubble induced calcium transient, presumably through direct competition with ESL macromolecules for interfacial occupancy, thus attenuating the interactions that trigger potentially deleterious biochemical pathways.

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Section: Introductionmentioning

confidence: 83%

Mechanotransductional basis of endothelial cell response to intravascular bubbles

et al. 2011

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“…The shear stresses and microjets produced by oscillating bubbles in a microvessel can directly impact the physiological functions of endothelial cells, red blood cells, and platelets. This results in vasocontraction, blood clot formation, and hemorrhage2627323334353637. The mechanism is similar to that of PDT and AVUT where microvessels are also destroyed by triggering the physiological functions of endothelial cells, red blood cells, and platelets.…”

mentioning

confidence: 96%

High-precision, non-invasive anti-microvascular approach via concurrent ultrasound and laser irradiation

Zhang

Mordovanakis

et al. 2017

Sci Rep

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Antivascular therapy represents a proven strategy to treat angiogenesis. By applying synchronized ultrasound bursts and nanosecond laser irradiation, we developed a novel, selective, non-invasive, localized antivascular method, termed photo-mediated ultrasound therapy (PUT). PUT takes advantage of the high native optical contrast among biological tissues and can treat microvessels without causing collateral damage to the surrounding tissue. In a chicken yolk sac membrane model, under the same ultrasound parameters (1 MHz at 0.45 MPa and 10 Hz with 10% duty cycle), PUT with 4 mJ/cm2 and 6 mJ/cm2 laser fluence induced 51% (p = 0.001) and 37% (p = 0.018) vessel diameter reductions respectively. With 8 mJ/cm2 laser fluence, PUT would yield vessel disruption (90%, p < 0.01). Selectivity of PUT was demonstrated by utilizing laser wavelengths at 578 nm or 650 nm, where PUT selectively shrank veins or occluded arteries. In a rabbit ear model, PUT induced a 68.5% reduction in blood perfusion after 7 days (p < 0.001) without damaging the surrounding cells. In vitro experiments in human blood suggested that cavitation may play a role in PUT. In conclusion, PUT holds significant promise as a novel non-invasive antivascular method with the capability to precisely target blood vessels.

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“…For the present study, two values of λ, namely, 0.9 and 1 are considered that represent nearly occluding bubble sizes. Our recent study (24) has shown that the hydrodynamic interactions between the finite sized bubble and the vessel wall remained nearly invariant for any further increases in bubble size beyond λ > 1.…”

Section: Methodsmentioning

confidence: 93%

“…While the previous work is limited to low fluid to gas viscosity ratios, the numerical methodology has been extended to solve the motion of a real gas bubble (27). The dynamics responsible for causing EC injury due to the motion of gas embolism has been clearly elucidated for the first time (24–26). In (33), the computational simulations of bubble motion included the presence and transport of soluble surfactants both in the bulk and the blood-bubble surface.…”

Section: Introductionmentioning

confidence: 99%

Computational Simulation of Hematocrit Effects on Arterial Gas Embolism Dynamics

Mukundakrishnan¹,

Ayyaswamy²,

Eckmann³

2012

aviat space environ med

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Background Recent computational investigations have shed light into the various hydrodynamic mechanisms at play during arterial gas embolism that may result in endothelial cell (EC) injury. Other recent studies have suggested that variations in hematocrit level may play an important role in determining the severity of neurological complications due to decompression sickness associated with gas embolism. Methods Towards developing a comprehensive picture, we have computationally modeled the effect of hematocrit variations on the motion of a nearly occluding gas bubble in arterial blood vessels of various sizes. The computational methodology is based on an axisymmetric finite difference immersed boundary numerical method to precisely track the blood-bubble dynamics of the interface. Hematocrit variations are taken to be in the range 0.2–0.6. The chosen blood vessel sizes correspond to small arteries, and small and large arterioles in normal humans. Results Relevant hydrodynamic interactions between the gas bubble and EC-lined vessel lumen have been characterized and quantified as a function of hematocrit levels. In particular, the variations in shear stress, spatial and temporal shear stress gradients, and the gap between bubble and vascular endothelium surfaces that contribute to EC injury have been computed. Discussion The results suggest that in small arteries, the deleterious hydrodynamic effects of the gas embolism on EC-lined cell wall are significantly amplified as the hematocrit levels increase. However, such pronounced variations with hematocrit levels are not observed in the arterioles.

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Bubble Motion in a Blood Vessel: Shear Stress Induced Endothelial Cell Injury

Cited by 39 publications

References 21 publications

Mechanotransductional basis of endothelial cell response to intravascular bubbles

Mechanotransductional basis of endothelial cell response to intravascular bubbles

High-precision, non-invasive anti-microvascular approach via concurrent ultrasound and laser irradiation

Computational Simulation of Hematocrit Effects on Arterial Gas Embolism Dynamics

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