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From the Departments of Neurosurgery (R.M.D., J.W.B. vd S., K.A.F.T.) and
Neurology (H.B. vd W.), University Hospital Utrecht; Department of In Vivo
Nuclear Magnetic Resonance, Bijvoet Center for Biomolecular Research, Utrecht
University (R.M.D., K.N.); Department of Biological Psychiatry, Groningen
University (S.K., G.J.T.H.); and Department of Pharmacology, Rudolf Magnus
Institute for Neurosciences, Utrecht University (D.J.D.W.) (Netherlands).
Correspondence to Rick M. Dijkhuizen, Department of In Vivo NMR, Bijvoet Center for Biomolecular Research, Utrecht University, Bolognalaan 50, NL-3584 CJ Utrecht, Netherlands. E-mail dijkhuiz{at}bijvoet.ruu.nl
Background and Purpose—Selective
regional sensitivity and delayed damage in cerebral ischemia
provide opportunities for directed and late therapy for stroke. Our aim
was to characterize the spatial and temporal profile of
ischemia-induced changes in cerebral perfusion and tissue
status, with the use of noninvasive MRI techniques, to gain more
insight in region-specific vulnerability and delayed damage.
Methods—Rats underwent 20 minutes of unilateral cerebral
hypoxia-ischemia (HI). We performed combined repetitive
quantitative diffusion-weighted, T2-weighted, and dynamic
susceptibility contrast-enhanced MRI from before HI to 5 hours after
HI. Data were correlated with parallel blood
oxygenation level–dependent MRI and laser-Doppler
flowmetry. Finally, MRI and histology were done 24 and 72 hours
after HI.
Results—Severe hypoperfusion during HI caused acute reductions of
the apparent diffusion coefficient (ADC) of tissue water in the
ipsilateral hemisphere. Reperfusion resulted in dynamic perfusion
alterations that varied spatially. The ADC recovered completely within
1 hour in the hippocampus (from 0.68±0.07 to
0.83±0.09x10-3 mm2/s), cortex (from
0.56±0.06 to 0.77±0.07x10-3 mm2/s),
and caudate putamen (from 0.58±0.06 to
0.75±0.06x10-3 mm2/s) but only
partially or not at all in the thalamus (from 0.65±0.07 to
0.68±0.12x10-3 mm2/s) and substantia
nigra (from 0.80±0.08 to 0.76±0.10x10-3
mm2/s). Secondary ADC reductions, accompanied by
significant T2 elevations and histological damage, were
observed after 24 hours. Initial and secondary ADC decreases were
observed invariably in the hippocampus, cortex, and caudate putamen and
in approximately 70% of the animals in the thalamus and substantia
nigra.
Conclusions—Region-specific responses and delayed
ischemic damage after transient HI were demonstrated by MRI.
Acute reperfusion-induced normalization of ADCs appeared to poorly
predict ultimate tissue recovery since secondary, irreversible damage
developed eventually.
Genentech,
Inc,
Department of Neuroscience and Cardiovascular
Research,
South San Francisco, California
© 1998 American Heart Association, Inc.
Original Contributions
Dynamics of Cerebral Tissue Injury and Perfusion After Temporary Hypoxia-Ischemia in the Rat
Evidence for Region-Specific Sensitivity and Delayed Damage
Editorial Comment
Evidence for Region-Specific Sensitivity and Delayed Damage
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