<i>In vivo</i> quantification of blood velocity in mouse carotid and pulmonary arteries by ECG‐triggered 3D time‐resolved magnetic resonance angiography

Parzy, Elodie; Miraux, Sylvain; Franconi, Jean‐Michel; Thiaudière, Eric

doi:10.1002/nbm.1365

Cited by 26 publications

(22 citation statements)

References 29 publications

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“…We found a maximum flow velocity in the carotid arteries of about 35 cm/s, which is in good agreement with the MRI study by Parzy et al [25], who reported a vessel-averaged flow velocity of about 18 cm/s in the systolic heart phase. Maximum blood flow velocities up to 120 cm/s were reported at sites of mouse carotid artery plaque by means of pulse-wave Doppler [10].…”

Section: Discussionsupporting

confidence: 93%

MRI-determined carotid artery flow velocities and wall shear stress in a mouse model of vulnerable and stable atherosclerotic plaque

Bochove

Straathof

Krams

et al. 2010

Magn Reson Mater Phy

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Objectives We report here on the pre-clinical MRI characterization of an apoE−/− mouse model of stable and vulnerable carotid artery atherosclerotic plaques, which were induced by a tapered restriction (cast) around the artery. Specific focus was on the quantification of the wall shear stress, which is considered a key player in the development of the plaque phenotype. Materials and methods In vivo MRI was performed at 9.4 T. The protocol consisted of time-of-flight angiography, highresolution T1-and T2-weighted black-blood imaging and phase-contrast flow velocity imaging as function of time in the cardiac cycle. Wall shear stress was determined by fitting the flow profile to a quadratic polynomial. Results Time-of-flight angiography confirmed preservation of blood flow through the carotid arteries in all cases. T1-and T2-weighted MRI resulted in high-resolution images in which the position of the cast, luminal narrowing introduced by cast and plaque, as well as the arterial wall could be well identified. Laminar flow with low wall shear stress (11.2 ± 5.2 Pa) was measured upstream to the cast at the position of the vulnerable plaque. Downstream to the cast at the position of the stable plaque, the apparent velocities were low, which Conclusions Flow velocities and wall shear stress were successfully measured in this mouse model of stable and unstable plaque. The presented tools can be used to provide valuable insights in the pathogenesis of atherosclerosis.

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Section: Discussionsupporting

confidence: 93%

MRI-determined carotid artery flow velocities and wall shear stress in a mouse model of vulnerable and stable atherosclerotic plaque

Bochove

Straathof

Krams

et al. 2010

Magn Reson Mater Phy

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“…However, induction of oxidative damage in tissues distant from a tumor site requires a different mechanism, perhaps through the blood or the lymphatic system. Since it takes only seconds for blood to circulate throughout the body of a mouse [69], chemicals released from a tumor into the blood would be distributed to distant organs, assuming that blood did not contain compounds to neutralize them. Chemicals released from the tumor may be more stable ROS species, or any of a variety of inflammatory factors.…”

Section: Discussionmentioning

confidence: 99%

Systemic DNA damage accumulation under in vivo tumor growth can be inhibited by the antioxidant Tempol

et al. 2014

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Aims Recently we found that mice bearing subcutaneous non-metastatic tumors exhibited elevated levels of two types of complex DNA damage, i.e., double-strand breaks and oxidatively-induced clustered DNA lesions in various tissues throughout the body, both adjacent to and distant from the tumor site. This DNA damage was dependent on CCL2, a cytokine involved in the recruitment and activation of macrophages, suggesting that this systemic DNA damage was mediated via tumor-induced chronic inflammatory responses involving cytokines, activation of macrophages, and consequent free radical production. If free radicals are involved, then a diet containing an antioxidant may decrease the distant DNA damage. Results Here we repeated our standard protocol in cohorts of two syngeneic tumor-bearing C57BL/6NCr mice that were on a Tempol-supplemented diet. We show that double-strand break and oxidatively-induced clustered DNA lesion levels were considerably decreased, about 2-3 fold, in the majority of tissues studied from the tumor-bearing mice fed the antioxidant Tempol compared to the control tumor-bearing mice. Similar results were also observed in nude mice suggesting that the Tempol effects are independent of functioning adaptive immunity. Conclusions This is the first in vivo study demonstrating the effect of a dietary antioxidant on abscopal DNA damage in tissues distant from a localized source of genotoxic stress. These findings may be important for understanding the mechanisms of genomic instability and carcinogenesis caused by chronic stress-induced systemic DNA damage and for developing preventative strategies.

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“…We found little perturbations in blood flow dynamics ( Figure 2D; Online Movie II), with diastolic velocities of 4.4±0.6 cm/s that are consistent with those reported using ECG-gated MRI. 21 For subsequent imaging of atherosclerotic regions within the living carotid artery, we chose regions proximal to the bifurcation, in areas where plaques developed over time under proatherogenic conditions (Figure 2E and 2F; Online Movie III). In these areas, the stabilization procedure allowed efficient imaging of defined intravascular structures even at high magnification (Online Movie IV).…”

Section: Circulation Research February 28 2014mentioning

confidence: 99%

High-Resolution Imaging of Intravascular Atherogenic Inflammation in Live Mice

Chèvre

González-Granado

Megens

et al. 2014

Circulation Research

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Rationale:The inflammatory processes that initiate and propagate atherosclerosis remain poorly understood, largely because defining the intravascular behavior of immune cells has been technically challenging. Respiratory and pulsatile movements have hampered in vivo visualization of leukocyte accumulation in athero-prone arteries at resolutions achieved in other tissues.Objective: To establish and to validate a method that allows high-resolution imaging of inflammatory leukocytes and platelets within the carotid artery of atherosusceptible mice in vivo. Methods and Results:We have devised a procedure to stabilize the mouse carotid artery mechanically without altering blood dynamics, which dramatically enhances temporal and spatial resolutions using high-speed intravital microscopy in multiple channels of fluorescence. By applying this methodology at different stages of disease progression in atherosusceptible mice, we first validated our approach by assessing the recruitment kinetics of various leukocyte subsets and platelets in athero-prone segments of the carotid artery. The high temporal and spatial resolution allowed the dissection of both the dynamic polarization of and the formation of subcellular domains within adhered leukocytes. We further demonstrate that the secondary capture of activated platelets on the plaque is predominantly mediated by neutrophils. Finally, we couple this procedure with triggered 2-photon microscopy to visualize the 3-dimensional movement of leukocytes in intimate contact with the arterial lumen. Conclusions:

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In vivo quantification of blood velocity in mouse carotid and pulmonary arteries by ECG‐triggered 3D time‐resolved magnetic resonance angiography

Cited by 26 publications

References 29 publications

MRI-determined carotid artery flow velocities and wall shear stress in a mouse model of vulnerable and stable atherosclerotic plaque

MRI-determined carotid artery flow velocities and wall shear stress in a mouse model of vulnerable and stable atherosclerotic plaque

Systemic DNA damage accumulation under in vivo tumor growth can be inhibited by the antioxidant Tempol

High-Resolution Imaging of Intravascular Atherogenic Inflammation in Live Mice

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