(Stroke. 1995;26:2112-2119.)
© 1995 American Heart Association, Inc.
Articles |
From Cyceron, Biomedical Cyclotron Unit of Caen, University of Caen CNRS URA 1829, INSERM U320, CEA DSV/DRIPP, and University Hospital of Caen (France).
Correspondence to Omar Touzani, Cyceron (CNRS URA 1829), Boulevard Henri Becquerel, BP 5229, 14074 Caen Cedex, France.
Background and Purpose In the positron emission tomography literature, markedly hypometabolic brain tissue (oxygen metabolism <1.3 to 1.7 mL · 100 g-1 · min-1) has often been equated with irreversible damage in the human brain. By serial positron emission tomography measurements, we investigated the temporal evolution of the volume of severely hypometabolic brain tissue after permanent middle cerebral artery occlusion in anesthetized baboons with, as a perspective, the development of rational therapeutic strategies.
Methods Seven anesthetized and ventilated baboons underwent sequential positron emission tomography examinations with the 15O steady-state technique before and 1, 4, 7, and 24 hours and 14 to 29 days after occlusion. In each baboon the infarct volume was calculated by quantitative histological procedures after 19 to 41 days of occlusion.
Results The sequential measurement of regional oxygen
metabolism demonstrated an extension (for
24 hours) of
the volume of severely hypometabolic tissue as defined
by both absolute and relative metabolic thresholds, and
this profile of evolutivity is observed no matter the threshold used.
Mean (±SEM) infarction volume of 2.4±0.6 cm3 was
comparable to a tissue volume with oxygen consumption <40% of
contralateral metabolism. The volume of
hypometabolic tissue was essentially stable at the 1-,
4-, and 7-hour postocclusion studies, increased markedly at the 24-hour
study point, and increased even further in the chronic-stage study
(on average, 17 days after occlusion). The tissue that eventually
displayed a severely hypometabolic state at the final
measurement showed a significant decrease of oxygen
metabolism and cerebral blood flow at each time
analyzed. In that tissue, the oxygen extraction fraction
increased significantly at 1 hour (although not thereafter).
Conclusions The extension of severely hypometabolic volume after middle cerebral artery occlusion reinforces the concept of a dynamic penumbra and suggests the existence of a relatively large window of therapeutic opportunity in which it may be possible to develop neuroprotective strategies. Our study suggests that maximum infarct volume is determined at some time between 24 hours and 17 days after permanent middle cerebral artery occlusion in anesthetized baboons.
Key Words: cerebral blood flow neuroprotection tomography, emission-computed baboons
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