Inhomogeneous sodium accumulation in the ischemic core in rat focal cerebral ischemia by 23Na MRI.
ABSTRACT To test the hypotheses that (i) the regional heterogeneity of brain sodium concentration ([Na(+)](br)) provides a parameter for ischemic progression not available from apparent diffusion coefficient (ADC) data, and (ii) [Na(+)](br) increases more in ischemic cortex than in the caudate putamen (CP) with its lesser collateral circulation after middle cerebral artery occlusion in the rat.
(23)Na twisted projection MRI was performed at 3 Tesla. [Na(+)](br) was independently determined by flame photometry. The ischemic core was localized by ADC, by microtubule-associated protein-2 immunohistochemistry, and by changes in surface reflectivity.
Within the ischemic core, the ADC ratio relative to the contralateral tissue was homogeneous (0.63 +/- 0.07), whereas the rate of [Na(+)](br) increase (slope) was heterogeneous (P < 0.005): 22 +/- 4%/h in the sites of maximum slope versus 14 +/- 1%/h elsewhere (here 100% is [Na(+)](br) in the contralateral brain). Maximum slopes in the cortex were higher than in CP (P < 0.05). In the ischemic regions, there was no slope/ADC correlation between animals and within the same brain (P > 0.1). Maximum slope was located at the periphery of ischemic core in 8/10 animals.
Unlike ADC, (23)Na MRI detected within-core ischemic lesion heterogeneity.
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ABSTRACT: Tissue sodium concentration increases in irreversibly damaged (core) tissue following ischemic stroke and can potentially help to differentiate the core from the adjacent hypoperfused but viable penumbra. To test this, multinuclear hydrogen-1/sodium-23 magnetic resonance imaging (MRI) was used to measure the changing sodium signal and hydrogen-apparent diffusion coefficient (ADC) in the ischemic core and penumbra after rat middle cerebral artery occlusion (MCAO). Penumbra and core were defined from perfusion imaging and histologically defined irreversibly damaged tissue. The sodium signal in the core increased linearly with time, whereas the ADC rapidly decreased by >30% within 20[thinsp]minutes of stroke onset, with very little change thereafter (0.5-6[thinsp]hours after MCAO). Previous reports suggest that the time point at which tissue sodium signal starts to rise above normal (onset of elevated tissue sodium, OETS) represents stroke onset time (SOT). However, extrapolating core data back in time reJournal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 10/2014; · 5.46 Impact Factor
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ABSTRACT: This study addresses the spatial relation between local Na(+) and K(+) imbalances in the ischemic core in a rat model of focal ischemic stroke. Quantitative [Na(+)] and [K(+)] brain maps were obtained by (23)Na MRI and histochemical K(+) staining, respectively, and calibrated by emission flame photometry of the micropunch brain samples. Stroke location was verified by diffusion MRI, by changes in tissue surface reflectivity and by immunohistochemistry with microtubule-associated protein 2 antibody. Na(+) and K(+) distribution within the ischemic core was inhomogeneous, with the maximum [Na(+)] increase and [K(+)] decrease typically observed in peripheral regions of the ischemic core. The pattern of the [K(+)] decrease matched the maximum rate of [Na(+)] increase ('slope'). Some residual mismatch between the sites of maximum Na(+) and K(+) imbalances was attributed to the different channels and pathways involved in transport of the two ions. A linear regression of the [Na(+)]br vs. [K(+)]br in the samples of ischemic brain indicates that for each K(+) equivalent leaving ischemic tissue, 0.8±0.1 Eq, on average, of Na(+) enter the tissue. Better understanding of the mechanistic link between the Na(+) influx and K(+) egress would validate the (23)Na MRI slope as a candidate biomarker and a complementary tool for assessing ischemic damage and treatment planning.Brain research 06/2013; 1527:199-208. · 2.46 Impact Factor
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ABSTRACT: Sodium MRI (sMRI) has undergone a tremendous amount of technical development during the last two decades that makes it a suitable tool for the study of human pathology in the acute setting within the constraints of a clinical environment. The salient role of the sodium ion during impaired ATP production during the course of brain ischemia makes sMRI an ideal tool for the study of ischemic tissue viability during stroke. In this paper, the current limitations of conventional MRI for the determination of tissue viability during evolving brain ischemia are discussed. This discussion is followed by a summary of the known findings about the dynamics of tissue sodium changes during brain ischemia. A mechanistic model for the explanation of these findings is presented together with the technical requirements for its investigation using clinical MRI scanners. An illustration of the salient features of the technique is also presented using a nonhuman primate model of reversible middle cerebral artery occlusion.Translational Stroke Research. 06/2012; 3(2).