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Experimental imaging in excised mouse hearts using a liquid nitrogen-cooled RF coil. ( A ) Diffusion tensor imaging-based tracking of myocardial myofibers with 100 µm <t>3</t> <t>isotropic</t> spatial resolution allows for a visualization of the change of the transmural change of fiber orientation and high precision quantification of the myofiber helix angle. In an isoproterenol myocardial damage model, distinct change of myofiber orientation as represented by the helix angle in subendocardial regions was observed at different positions in the mouse heart (grey bars: control group. Red bars; isoproterenterol model). Reprinted under CC-BY license from . ( B ) DTI-based fiber-tracking in mouse aorta with 80 µm 3 isotropic spatial resolution allows for visualization of the orientation of intimal vascular smooth muscle cells. ( C ) T2-weighted imaging of an excised porcine aorta with 0.3 mm slice thickness allows for an almost histologic visualization of vascular anatomy. ( D ) Dynamic <t>MRI</t> in the excised aorta following exposition to 30 mM TEMPOL as an T1-modifying contrast agent. The TEMPOL-induced change of the T1 relaxation times from outside and inside the vessel allows for the study of its kinetics over time. As a proof of principle, the aorta was exposed to 20 mM ascorbic acid (ASA) after 40 min. ASA also diffuses into the vascular wall with a similar time constant. As it reduces the free electron of TEMPOL, T1-contrast vanishes completely at 50 min. This type of measurement may allow for imaging of vascular or myocardial oxidative stress. ( E ) MRI of a 2 mm long cardiac organoid. MRI at 20 × 20 × 70 µm 3 spatial resolution with the organoid exposed to buffer solution. The dark spot in the right image denotes an air bubble which also induces a slight susceptibility artefact. ( F ) Dynamic imaging of TEMPOL kinetics in the organoid of Fig. ( E ) after exposure of the organoid to TEMPOL dissolved within buffer. The red and the blue curves denote the temporal evolution of the MRI signal in two different regions, while the orange curve is a reference region in buffer. Please note that the buffer signal is higher than that the organoid because—other than in <xref ref-type=Figure 6E —buffer contained T1-shortening TEMPOL. " width="250" height="auto" />
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Chem Impex International buffer components
Experimental imaging in excised mouse hearts using a liquid nitrogen-cooled RF coil. ( A ) Diffusion tensor imaging-based tracking of myocardial myofibers with 100 µm <t>3</t> <t>isotropic</t> spatial resolution allows for a visualization of the change of the transmural change of fiber orientation and high precision quantification of the myofiber helix angle. In an isoproterenol myocardial damage model, distinct change of myofiber orientation as represented by the helix angle in subendocardial regions was observed at different positions in the mouse heart (grey bars: control group. Red bars; isoproterenterol model). Reprinted under CC-BY license from . ( B ) DTI-based fiber-tracking in mouse aorta with 80 µm 3 isotropic spatial resolution allows for visualization of the orientation of intimal vascular smooth muscle cells. ( C ) T2-weighted imaging of an excised porcine aorta with 0.3 mm slice thickness allows for an almost histologic visualization of vascular anatomy. ( D ) Dynamic <t>MRI</t> in the excised aorta following exposition to 30 mM TEMPOL as an T1-modifying contrast agent. The TEMPOL-induced change of the T1 relaxation times from outside and inside the vessel allows for the study of its kinetics over time. As a proof of principle, the aorta was exposed to 20 mM ascorbic acid (ASA) after 40 min. ASA also diffuses into the vascular wall with a similar time constant. As it reduces the free electron of TEMPOL, T1-contrast vanishes completely at 50 min. This type of measurement may allow for imaging of vascular or myocardial oxidative stress. ( E ) MRI of a 2 mm long cardiac organoid. MRI at 20 × 20 × 70 µm 3 spatial resolution with the organoid exposed to buffer solution. The dark spot in the right image denotes an air bubble which also induces a slight susceptibility artefact. ( F ) Dynamic imaging of TEMPOL kinetics in the organoid of Fig. ( E ) after exposure of the organoid to TEMPOL dissolved within buffer. The red and the blue curves denote the temporal evolution of the MRI signal in two different regions, while the orange curve is a reference region in buffer. Please note that the buffer signal is higher than that the organoid because—other than in <xref ref-type=Figure 6E —buffer contained T1-shortening TEMPOL. " width="250" height="auto" />
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Experimental imaging in excised mouse hearts using a liquid nitrogen-cooled RF coil. ( A ) Diffusion tensor imaging-based tracking of myocardial myofibers with 100 µm <t>3</t> <t>isotropic</t> spatial resolution allows for a visualization of the change of the transmural change of fiber orientation and high precision quantification of the myofiber helix angle. In an isoproterenol myocardial damage model, distinct change of myofiber orientation as represented by the helix angle in subendocardial regions was observed at different positions in the mouse heart (grey bars: control group. Red bars; isoproterenterol model). Reprinted under CC-BY license from . ( B ) DTI-based fiber-tracking in mouse aorta with 80 µm 3 isotropic spatial resolution allows for visualization of the orientation of intimal vascular smooth muscle cells. ( C ) T2-weighted imaging of an excised porcine aorta with 0.3 mm slice thickness allows for an almost histologic visualization of vascular anatomy. ( D ) Dynamic <t>MRI</t> in the excised aorta following exposition to 30 mM TEMPOL as an T1-modifying contrast agent. The TEMPOL-induced change of the T1 relaxation times from outside and inside the vessel allows for the study of its kinetics over time. As a proof of principle, the aorta was exposed to 20 mM ascorbic acid (ASA) after 40 min. ASA also diffuses into the vascular wall with a similar time constant. As it reduces the free electron of TEMPOL, T1-contrast vanishes completely at 50 min. This type of measurement may allow for imaging of vascular or myocardial oxidative stress. ( E ) MRI of a 2 mm long cardiac organoid. MRI at 20 × 20 × 70 µm 3 spatial resolution with the organoid exposed to buffer solution. The dark spot in the right image denotes an air bubble which also induces a slight susceptibility artefact. ( F ) Dynamic imaging of TEMPOL kinetics in the organoid of Fig. ( E ) after exposure of the organoid to TEMPOL dissolved within buffer. The red and the blue curves denote the temporal evolution of the MRI signal in two different regions, while the orange curve is a reference region in buffer. Please note that the buffer signal is higher than that the organoid because—other than in <xref ref-type=Figure 6E —buffer contained T1-shortening TEMPOL. " width="250" height="auto" />
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Image Search Results


Experimental imaging in excised mouse hearts using a liquid nitrogen-cooled RF coil. ( A ) Diffusion tensor imaging-based tracking of myocardial myofibers with 100 µm 3 isotropic spatial resolution allows for a visualization of the change of the transmural change of fiber orientation and high precision quantification of the myofiber helix angle. In an isoproterenol myocardial damage model, distinct change of myofiber orientation as represented by the helix angle in subendocardial regions was observed at different positions in the mouse heart (grey bars: control group. Red bars; isoproterenterol model). Reprinted under CC-BY license from . ( B ) DTI-based fiber-tracking in mouse aorta with 80 µm 3 isotropic spatial resolution allows for visualization of the orientation of intimal vascular smooth muscle cells. ( C ) T2-weighted imaging of an excised porcine aorta with 0.3 mm slice thickness allows for an almost histologic visualization of vascular anatomy. ( D ) Dynamic MRI in the excised aorta following exposition to 30 mM TEMPOL as an T1-modifying contrast agent. The TEMPOL-induced change of the T1 relaxation times from outside and inside the vessel allows for the study of its kinetics over time. As a proof of principle, the aorta was exposed to 20 mM ascorbic acid (ASA) after 40 min. ASA also diffuses into the vascular wall with a similar time constant. As it reduces the free electron of TEMPOL, T1-contrast vanishes completely at 50 min. This type of measurement may allow for imaging of vascular or myocardial oxidative stress. ( E ) MRI of a 2 mm long cardiac organoid. MRI at 20 × 20 × 70 µm 3 spatial resolution with the organoid exposed to buffer solution. The dark spot in the right image denotes an air bubble which also induces a slight susceptibility artefact. ( F ) Dynamic imaging of TEMPOL kinetics in the organoid of Fig. ( E ) after exposure of the organoid to TEMPOL dissolved within buffer. The red and the blue curves denote the temporal evolution of the MRI signal in two different regions, while the orange curve is a reference region in buffer. Please note that the buffer signal is higher than that the organoid because—other than in <xref ref-type=Figure 6E —buffer contained T1-shortening TEMPOL. " width="100%" height="100%">

Journal: Frontiers in Cardiovascular Medicine

Article Title: Ultra-high field cardiac MRI in large animals and humans for translational cardiovascular research

doi: 10.3389/fcvm.2023.1068390

Figure Lengend Snippet: Experimental imaging in excised mouse hearts using a liquid nitrogen-cooled RF coil. ( A ) Diffusion tensor imaging-based tracking of myocardial myofibers with 100 µm 3 isotropic spatial resolution allows for a visualization of the change of the transmural change of fiber orientation and high precision quantification of the myofiber helix angle. In an isoproterenol myocardial damage model, distinct change of myofiber orientation as represented by the helix angle in subendocardial regions was observed at different positions in the mouse heart (grey bars: control group. Red bars; isoproterenterol model). Reprinted under CC-BY license from . ( B ) DTI-based fiber-tracking in mouse aorta with 80 µm 3 isotropic spatial resolution allows for visualization of the orientation of intimal vascular smooth muscle cells. ( C ) T2-weighted imaging of an excised porcine aorta with 0.3 mm slice thickness allows for an almost histologic visualization of vascular anatomy. ( D ) Dynamic MRI in the excised aorta following exposition to 30 mM TEMPOL as an T1-modifying contrast agent. The TEMPOL-induced change of the T1 relaxation times from outside and inside the vessel allows for the study of its kinetics over time. As a proof of principle, the aorta was exposed to 20 mM ascorbic acid (ASA) after 40 min. ASA also diffuses into the vascular wall with a similar time constant. As it reduces the free electron of TEMPOL, T1-contrast vanishes completely at 50 min. This type of measurement may allow for imaging of vascular or myocardial oxidative stress. ( E ) MRI of a 2 mm long cardiac organoid. MRI at 20 × 20 × 70 µm 3 spatial resolution with the organoid exposed to buffer solution. The dark spot in the right image denotes an air bubble which also induces a slight susceptibility artefact. ( F ) Dynamic imaging of TEMPOL kinetics in the organoid of Fig. ( E ) after exposure of the organoid to TEMPOL dissolved within buffer. The red and the blue curves denote the temporal evolution of the MRI signal in two different regions, while the orange curve is a reference region in buffer. Please note that the buffer signal is higher than that the organoid because—other than in Figure 6E —buffer contained T1-shortening TEMPOL.

Article Snippet: Hearts were then sent to Wuerzburg for high resolution (100 µm isotropic) ex-vivo DTI at the Bruker MRI system.

Techniques: Imaging, Diffusion-based Assay