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Reexamination of Hyperoxia in Ischemic-Stroke Treatment

Hyperoxia treatment of acute stroke can be neuroprotective, but only when initiated within a narrow time frame after stroke onset, this study shows.

These researchers undertook two potentially important experimental stroke studies to investigate whether hyperoxia decreases acute ischemic-stroke lesion volume. They used the filament model to induce 2-hour middle cerebral artery occlusion (MCAO) in 38 rats.

First, they compared the effects of hyperoxia treatment (FiO₂, 100%) to those of normoxia (FiO₂, 30%). They measured changes in pathology and in serial diffusion- and perfusion-weighted MRI (DWI and PWI), as well as changes in diffusion of water using the apparent diffusion coefficient (ADC) and changes in cerebral blood flow (CBF) using continuous laser-Doppler flowmetry. Second, animals were randomized to normoxia or hyperoxia treatment starting at 15, 30, or 45 minutes after MCAO onset and ending 15 minutes after reperfusion (2 hours after MCAO onset).

Hyperoxia reduced ADC lesions, but the reduction was not sustained beyond 2 hours. When hyperoxia was started 30 minutes or sooner after MCAO onset, total and cortical stroke volumes were significantly reduced 48 hours after stroke onset. CBF was reduced in all cases and did not influence stroke volume. The authors conclude that early hyperoxia therapy (begun less than 30 minutes after stroke onset) is neuroprotective. However, they note the well-known potential untoward effects of hyperoxia and hyperbaric oxygen therapy (HBO) on CBF, on the vasculature, and on free-radical formation.

Comment: Use of HBO or hyperoxia in acute ischemic stroke has been controversial. The current research may explain why results in the past have been inconsistent, even contradictory. The crucial finding is the rather narrow time window for benefit, even while ischemia remains. These provocative studies deserve consideration by clinicians who treat acute ischemic stroke.

Also, stroke investigators should conduct a randomized, prospective study of hyperoxia, particularly in conjunction with tissue plasminogen activator (which would simulate the current study's model), or in ischemic strokes acutely. These studies should also be designed to quantify the stroke lesion using DWI, PWI, and ADC, which likely will become standard in evaluating acute ischemic-stroke therapies, as will FLAIR (fluid attenuation inversion recovery) and MRS (magnetic resonance spectroscopy) where available. An HBO protocol for acute ischemic stroke is in the final planning stages (Principal Investigator, James F. Toole, Wake Forest University). Given the current findings, the protocol of repeated HBO exposures may need modification in favor of early, sustained HBO.

— Frank M. Yatsu, MD

Dr. Yatsu is Professor, Department of Neurology, University of Texas, Houston, Medical School.

Published in Journal Watch Neurology July 12, 2002

Citation(s):

Singhal AB et al. Normobaric hyperoxia reduces MRI diffusion abnormalities and infarct size in experimental stroke. Neurology 2002 Mar 26; 58:945-52.

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