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High temporal resolution parametric MRI monitoring of the initial ischemia/reperfusion phase in experimental acute kidney injury.

Pohlmann A, Hentschel J, Fechner M, Hoff U, Bubalo G, Arakelyan K, Cantow K, Seeliger E, Flemming B, Waiczies H, Waiczies S, Schunck WH, Dragun D, Niendorf T - PLoS ONE (2013)

Bottom Line: There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI.Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats.This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

View Article: PubMed Central - PubMed

Affiliation: Berlin Ultrahigh Field Facility, Max Delbrück Center for Molecular Medicine, Berlin, Germany. andreas.pohlmann@mdc-berlin.de

ABSTRACT
Ischemia/reperfusion (I/R) injury, a consequence of kidney hypoperfusion or temporary interruption of blood flow is a common cause of acute kidney injury (AKI). There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI. Non-invasive in vivo parametric magnetic resonance imaging (MRI) may elucidate spatio-temporal pathophysiological changes in the kidney by monitoring the MR relaxation parameters T2* and T2, which are known to be sensitive to blood oxygenation. The aim of our study was to establish the technical feasibility of fast continuous T2*/T2 mapping throughout renal I/R. MRI was combined with a remotely controlled I/R model and a segmentation model based semi-automated quantitative analysis. This technique enabled the detailed assessment of in vivo changes in all kidney regions during ischemia and early reperfusion. Significant changes in T2* and T2 were observed shortly after induction of renal ischemia and during the initial reperfusion phase. Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats. This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

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Hypoxia and hyperoxia experiments: T2*-weighted MR images (gray scale) and T2* parameter maps (color-coded) derived from MGE acquisitions.Following two baseline measurements of T2*, hypoxia/hyperoxia was induced by changing the inhaled gas mixture from air to 10%/90% O2/N2 or 100% O2. T2*/T2 measurements were repeated directly after and exactly 5 minutes after onset of hypoxia/hyperoxia (to ensure equal timing of the MR scans). Subsequently inhaled gas was changed back to air and T2*/T2 monitored continuously for another ∼9 minutes.
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pone-0057411-g002: Hypoxia and hyperoxia experiments: T2*-weighted MR images (gray scale) and T2* parameter maps (color-coded) derived from MGE acquisitions.Following two baseline measurements of T2*, hypoxia/hyperoxia was induced by changing the inhaled gas mixture from air to 10%/90% O2/N2 or 100% O2. T2*/T2 measurements were repeated directly after and exactly 5 minutes after onset of hypoxia/hyperoxia (to ensure equal timing of the MR scans). Subsequently inhaled gas was changed back to air and T2*/T2 monitored continuously for another ∼9 minutes.

Mentions: A respiratory mask was used, which provided air (normoxia) at a flow rate of 1000 ml/min. Following baseline measurements of T2*/T2, hypoxia was induced by adjusting the gas mixture to 10/90% O2/N2. T2*/T2 measurements were conducted throughout 8 minutes after induction of hypoxia. The final T2*/T2 scans during hypoxia were started exactly 5 minutes after hypoxia onset, to ensure equal hypoxia durations and comparable timing of the MR scans. On completion of these MR scans, inhaled gas mixture was changed back to air and T2*/T2 continuously monitored for another ∼9 minutes. The same protocol was followed for the hyperoxia experiments by setting the inhaled gas to 100% O2. Figure 2 illustrates the experimental procedure, by showing the timeline and the corresponding T2*-weighted MR images together with calculated T2* parameter maps acquired prior, during and after hypoxia/hyperoxia.


High temporal resolution parametric MRI monitoring of the initial ischemia/reperfusion phase in experimental acute kidney injury.

Pohlmann A, Hentschel J, Fechner M, Hoff U, Bubalo G, Arakelyan K, Cantow K, Seeliger E, Flemming B, Waiczies H, Waiczies S, Schunck WH, Dragun D, Niendorf T - PLoS ONE (2013)

Hypoxia and hyperoxia experiments: T2*-weighted MR images (gray scale) and T2* parameter maps (color-coded) derived from MGE acquisitions.Following two baseline measurements of T2*, hypoxia/hyperoxia was induced by changing the inhaled gas mixture from air to 10%/90% O2/N2 or 100% O2. T2*/T2 measurements were repeated directly after and exactly 5 minutes after onset of hypoxia/hyperoxia (to ensure equal timing of the MR scans). Subsequently inhaled gas was changed back to air and T2*/T2 monitored continuously for another ∼9 minutes.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3585384&req=5

pone-0057411-g002: Hypoxia and hyperoxia experiments: T2*-weighted MR images (gray scale) and T2* parameter maps (color-coded) derived from MGE acquisitions.Following two baseline measurements of T2*, hypoxia/hyperoxia was induced by changing the inhaled gas mixture from air to 10%/90% O2/N2 or 100% O2. T2*/T2 measurements were repeated directly after and exactly 5 minutes after onset of hypoxia/hyperoxia (to ensure equal timing of the MR scans). Subsequently inhaled gas was changed back to air and T2*/T2 monitored continuously for another ∼9 minutes.
Mentions: A respiratory mask was used, which provided air (normoxia) at a flow rate of 1000 ml/min. Following baseline measurements of T2*/T2, hypoxia was induced by adjusting the gas mixture to 10/90% O2/N2. T2*/T2 measurements were conducted throughout 8 minutes after induction of hypoxia. The final T2*/T2 scans during hypoxia were started exactly 5 minutes after hypoxia onset, to ensure equal hypoxia durations and comparable timing of the MR scans. On completion of these MR scans, inhaled gas mixture was changed back to air and T2*/T2 continuously monitored for another ∼9 minutes. The same protocol was followed for the hyperoxia experiments by setting the inhaled gas to 100% O2. Figure 2 illustrates the experimental procedure, by showing the timeline and the corresponding T2*-weighted MR images together with calculated T2* parameter maps acquired prior, during and after hypoxia/hyperoxia.

Bottom Line: There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI.Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats.This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

View Article: PubMed Central - PubMed

Affiliation: Berlin Ultrahigh Field Facility, Max Delbrück Center for Molecular Medicine, Berlin, Germany. andreas.pohlmann@mdc-berlin.de

ABSTRACT
Ischemia/reperfusion (I/R) injury, a consequence of kidney hypoperfusion or temporary interruption of blood flow is a common cause of acute kidney injury (AKI). There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI. Non-invasive in vivo parametric magnetic resonance imaging (MRI) may elucidate spatio-temporal pathophysiological changes in the kidney by monitoring the MR relaxation parameters T2* and T2, which are known to be sensitive to blood oxygenation. The aim of our study was to establish the technical feasibility of fast continuous T2*/T2 mapping throughout renal I/R. MRI was combined with a remotely controlled I/R model and a segmentation model based semi-automated quantitative analysis. This technique enabled the detailed assessment of in vivo changes in all kidney regions during ischemia and early reperfusion. Significant changes in T2* and T2 were observed shortly after induction of renal ischemia and during the initial reperfusion phase. Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats. This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

Show MeSH
Related in: MedlinePlus