Late Reversal of Cerebral Perfusion and Water Diffusion after Transient Focal Ischemia in Rats

Wang, Lei; Yushmanov, Victor E.; Liachenko, Serguei; Tang, Pei; Hamilton, Ronald L.; Xu, Yan

doi:10.1097/00004647-200203000-00002

Cited by 29 publications

(35 citation statements)

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“…In the present work, the lower T 2 regions in the ipsilateral hemisphere as compared to the contralateral one were observed in some of the animals within 3-4 h of permanent occlusion. T 2 -hyperintensity was observed in the ipsilateral caudate putamen, frontoparietal cortex, and thalamus in both permanent and transient experiments after 24 -100 h of MCAO (42). In a recent study (15), an early drop in T 2 (within a few minutes post-MCAO) followed by a gradual linear increase in occluded areas during about 5 h was also observed.…”

Section: Discussionmentioning

confidence: 83%

ADC characterization of region‐specific response to cerebral perfusion deficit in rats by MRI at 9.4 T

Yushmanov

Wang

Liachenko

et al. 2002

Magnetic Resonance in Med

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Region-specific cerebral blood flow (CBF) and apparent diffusion coefficient (ADC) of water in the rat brain were quantified in vivo by high-field MRI (9.4 T) for 6 -7 h after middle cerebral artery occlusion (MCAO). Upon occlusion, average CBF fell from about 1.5-2 ml/g/min to below 0.5 ml/g/min in cortical areas and the amygdala, and below 0. The apparent diffusion coefficient (ADC) of water, which is measurable noninvasively by MRI, has been proposed as a reliable parameter for early detection of brain ischemia (1-3). ADC was shown to be sensitive to acute ischemia within minutes of occurrence (4). Currently, the intraluminal thread model of middle cerebral artery occlusion (MCAO) in rats (5-7) is generally accepted as a standard model of focal cerebral ischemia. In this model, cerebral blood flow (CBF) measurements are usually carried out to determine adequate occlusion (in both permanent and transient MCAO models) and reperfusion (in the transient model) (8 -14). When describing quantitative changes in cerebral perfusion and ADC values, data are usually reported as averages over 1) very small local regions (of several pixels in size) inside the involved brain structures (9,11), or 2) the whole lesion region, with reference to the symmetric contralateral region or to the whole contralateral hemisphere (12,15).In perfusion and ADC studies with the MCAO model in rats, two issues deserve further elaboration. First, the detailed regional dynamics of ADC and CBF, averaged over specific macroscopic brain regions, remains for the most part unexplored. Second, variability in experimental approaches and animals used in the studies results in a certain diversity of experimental findings. Even more important is that the definition of occlusion based on perfusion measurements is not always sufficiently rigorous, and may lead to different cellular responses in the occluded area. To characterize ischemic damage more quantitatively, stringent criteria are needed. An ADC-based definition of occlusion appears to be more adequate, since it is associated with cellular response to ischemia. This feature also makes ADC a suitable candidate for clinical use.CBF measurements are usually performed by laser-Doppler flowmetry (8,14,16) or perfusion-weighted magnetic resonance imaging (MRI). Qualitative perfusion-weighted images may be produced using paramagnetic contrast agents and echo-planar imaging (EPI) (bolus-tracking), and relative CBF indexes may be obtained (11-13). An alternative technique has been developed that uses arterial spin tagging and thus does not need any exogenous contrast agents (17). The arterial spin tagging technique was shown to be suitable for noninvasive quantitative measurements of CBF (17)(18)(19). MRI at high magnetic field (7 T and above) ensures better sensitivity in perfusion measurements (20). The variability in magnetic fields, however, may contribute to lower consistency in results obtained, especially when the difference in magnetic relaxation times is concerned.Variability in animal responses to...

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Section: Discussionmentioning

confidence: 83%

ADC characterization of region‐specific response to cerebral perfusion deficit in rats by MRI at 9.4 T

Yushmanov

Wang

Liachenko

et al. 2002

Magnetic Resonance in Med

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“…It is feasible that better collateral circulation and milder hypoperfusion in the former underlies this effect. 20 Delayed maturation of the cortical lesion is likely an intrinsic tissular effect, but we cannot exclude a contribution of the previous striatal lesion to triggering manifestation of the cortical lesion.…”

Section: Discussionmentioning

confidence: 90%

Modest MRI Signal Intensity Changes Precede Delayed Cortical Necrosis After Transient Focal Ischemia in the Rat

Rojas

Martín²,

Justicia

et al. 2006

Stroke

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Background and Purpose-Diffusion-weighted imaging (DWI) hyperintensities and apparent diffusion coefficient (ADC) hypointensities are MRI features of acute stroke. DWI alterations during ischemia recover with early reperfusion, but they can reappear later. Pronounced signal abnormalities early after stroke are associated with infarction, but the significance of subtle changes is unclear. Here we evaluated the degree and time course of regional signal intensity changes during the first 24 hours of reperfusion after transient ischemia, and we related them to the progression of the histopathological damage. Methods-Rats (nϭ54) were subjected to 1-hour intraluminal middle cerebral artery occlusion to assess the dynamics of MRI signal intensity changes during the initial 24 hours and their correspondent histopathological features: 2,3,5-triphenyltetrazolium chloride (TTC) staining, and hematoxylin and eosin, and immunoreactivity to 70-kDa heat shock protein and to astroglial and microglial markers. Results-This model of ischemia caused early striatal infarction but delayed necrosis in the cortex. The striatum showed marked MRI changes from 4 hours of reperfusion. By 12 hours, the striatal ADC signal intensity ratio to the homologous contralateral region was 30% reduced, and the TTC staining evidenced infarction. Contrarily, the cortical ADC ratio was only 15% reduced, and TTC staining was normal at 12 hours. After this time, the cortex showed sudden and pronounced (Ͼ30%) ADC signal intensity changes coincidentally with the manifestation of infarction, accompanied with severe vacuolation and unambiguous signs of neuronal and astroglial death. Conclusions-These findings suggest that minor changes in ADC signal intensity early after ischemia should not be underestimated because they may be harbingers of delayed infarction.

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“…This suggests excellent development of collaterals following the carotid artery occlusion [34]. A few recent studies in adults have also reported a hyperperfusion at relatively chronic recovery times (24-96 h) after transient hypoxia/ischemia [9,11,31]. Whether such hyperemia is beneficial or has adverse effects is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The blood flow response following transient hypoxia and/or ischemia can vary from hyper-to hypoperfusion, where hyperemia has been considered to have either beneficial or adverse effects whereas cerebral hypoperfusion may lead to secondary energy failure or simply be a consequence of reduced metabolic requirements of injured tissue [7,[9][10][11][12][13]. Age-dependent changes in various cerebral functions including the autoregulatory flow-response, bloodbrain barrier function and receptor and synaptic activity have been quite well studied [1,3,14].…”

Section: Introductionmentioning

confidence: 99%

Cerebral blood flow response to a hypoxic-ischemic insult differs in neonatal and juvenile rats

Qiao

Latta

Foniok

et al. 2004

MAGMA

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To compare the cerebral blood flow (CBF) response to a transient episode of hypoxia-ischemia producing damage in neonatal and juvenile rats. One- and four-week-old rats were subjected to unilateral carotid artery occlusion plus hypoxia (8% oxygen). Perfusion MR images were acquired either in sham controls or in hypoxic-ischemic rats before, during, 1 h and 24 h after hypoxia-ischemia. At 24 h post hypoxia-ischemia, T2 maps and histology were used to assess damage. In sham controls, CBF increased twofold between the age of one and four weeks. Reductions in CBF ipsilateral to the occlusion occurred during hypoxia-ischemia followed by a substantial recovery at 1 h post in both age groups. However, contralaterally, hyperemia occurred during hypoxia-ischemia in four-week but not one-week-old rats. Similarly, hyperemia occurred ipsilaterally at 24 h post hypoxia-ischemia in four-week but not one-week-olds, corresponding to the distribution of elevations in T2. Despite CBF differences, extensive cell death occurred ipsilaterally in both age groups. The CBF responses to hypoxia-ischemia and reperfusion differ depending on postnatal age, with hyperemia occurring in juvenile but not neonatal rats. The results suggest a greater CBF responsiveness and differential relationship between post-ischemic vascular perfusion and tissue injury in older compared with immature animals.

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Late Reversal of Cerebral Perfusion and Water Diffusion after Transient Focal Ischemia in Rats

Cited by 29 publications

References 50 publications

ADC characterization of region‐specific response to cerebral perfusion deficit in rats by MRI at 9.4 T

ADC characterization of region‐specific response to cerebral perfusion deficit in rats by MRI at 9.4 T

Modest MRI Signal Intensity Changes Precede Delayed Cortical Necrosis After Transient Focal Ischemia in the Rat

Cerebral blood flow response to a hypoxic-ischemic insult differs in neonatal and juvenile rats

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