Sodium T2*-weighted MR imaging of acute focal cerebral ischemia in rabbits

Regional and temporal variations in tissue sodium concentration during the acute stroke phase

“…A recent article reported no 23 increase in penumbral tissue as defined by the diffusion/perfusion-mismatch within 4-7 h after stroke onset (25). In the ischemic core (not defined as cortex or subcortex) in a rabbit embolic model, an acute (11%) decrease in signal during the first 40 min of ischemia was followed by a 12%/h increase, culminating in a 25% increase over baseline by 4 h poststroke (15). The measured TSC slopes of 22%/h (CN) and 23%/h (COR) in this study compared well with 25%/h (11) and 24%/h (13) measured in rat ischemic cortex following MCAO plus bilateral common carotid artery occlusion and intraluminal filament-induced MCAO, respectively.…”

“…Recent studies using 23 Na-MRI have succeeded in noninvasively measuring an increase in TSC for up to 3 days after stroke induction with moderate spatial-temporal resolution in various animal stroke models (4,(10)(11)(12)(13)(14). However, significant differences were reported in the specific time-course of the TSC after cerebral ischemia in these studies, with measurements varying between a direct increase (11,14), and a delayed increase with either an initial decrease (15) or with only a slightly increasing TSC (1,9) during the early phase. Furthermore, to our knowledge, no study to date has succeeded in quantifying the TSC in different ischemic subregions (i.e., penumbra and core) during the early hours of stroke.…”

“…Furthermore, to our knowledge, no study to date has succeeded in quantifying the TSC in different ischemic subregions (i.e., penumbra and core) during the early hours of stroke. 23 Na-MRI studies in animal stroke models have made use of a variety of models, including: the intraluminal thread model (13,14), direct middle cerebral artery occlusion (MCAO) with combined bilateral common carotid artery occlusion (11,13) in the rat, and autologous embolic MCAO models in rabbit (15) and nonhuman primate (1,9). These models induced different severities of ischemic insult, depending on the addition of common carotid artery occlusion, the level of collateral blood supply in the model and the neuroanatomical location of the region of interest (ROI) (e.g., ischemic core versus penumbra) with resulting differences in TSC.…”

“…These models induced different severities of ischemic insult, depending on the addition of common carotid artery occlusion, the level of collateral blood supply in the model and the neuroanatomical location of the region of interest (ROI) (e.g., ischemic core versus penumbra) with resulting differences in TSC. In one study where acute 23 Na signal data was measured in one animal (from 20-min poststroke), an initial decrease in 23 Na was detected before increasing 23 Na in tissue destined to die (15). A common feature of the majority of these studies was the lack of quantification of the TSC, due to the achieved low signal/noise ratio (SNR) values.…”

Proton and sodium MRI assessment of fluid level in calf tissue

“…However, since the proton MR signal consists of both extra-and intracellular water molecules, and more water is contained within the intracellular compartment in many parts of the body, proton MRI alone may not be an optimal tool for assessing changes in ECW:ICW distribution. Based on the fact that sodium stays predominantly in the extracellular compartment (4) and its MR signal is sensitive to changes in physiological conditions (17)(18)(19), we hypothesized that sodium MRI would be highly sensitive for monitoring fluid level changes within extracellular compartments. The purpose of this study was to investigate the feasibility of using both proton and sodium MRI to detect changes of fluid level in the calf and the localized ECW:ICW ratio.…”