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on May 21, 2009

Stroke. 2009
Published online before print May 21, 2009, doi: 10.1161/STROKEAHA.109.548453
A more recent version of this article appeared on July 1, 2009
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Submitted on February 12, 2009
Revised on March 26, 2009
Accepted on April 15, 2009

Faster Recovery of Cerebral Perfusion in SOD1-Overexpressed Rats After Cardiac Arrest and Resuscitation

Yan Xu PhD*; Serguei M. Liachenko; Pei Tang PhD; and Pak H. Chan PhD

From the Departments of Anesthesiology (Y.X., S.M.L., P.T.), Pharmacology and Chemical Biology (Y.X., P.T.), Structural Biology (Y.X.), and Computational Biology (P.T.), University of Pittsburgh School of Medicine, Pa; and the Departments of Neurosurgery (P.H.C.) and Neurology and Neurological Sciences (P.H.C.), Stanford University School of Medicine, Stanford, Calif.

* To whom correspondence should be addressed. E-mail: xuy{at}anes.upmc.edu.

Background and Purpose—Protracted hypoperfusion is one of the hallmarks of secondary cerebral derangement after cardiac arrest and resuscitation (CAR), and reactive oxygen species have been implicated in reperfusion abnormalities.

Methods—Using transgenic (Tg) rats overexpressing copper zinc superoxide dismutase (SOD1), we investigated the role of this intrinsic antioxidant in the restoration of cerebral blood flow (CBF) after CAR. Nine Tg and 11 wild-type (WT) rats were subjected to a nominal 15-minute cardiac arrest, and CBF was measured using the noninvasive arterial spin labeling MRI method before and during cardiac arrest, and 0 to 2 hours and 1 to 5 days after resuscitation.

Results—The SOD1-Tg rats showed rapid normalization of CBF 1 day after the insult, whereas CBF in WT animals remained abnormal for at least 5 days, showing a progressive increase in CBF from hypo- to hyperperfusion on postresuscitation days 1 to 5. The long-term outcome, as measured by survival time, change in body weight, and mapping of apparent diffusion coefficient (ADC) for ion/water homeostasis, was significantly better in the SOD1-Tg rats.

Conclusion—Our results support the notion that reactive oxygen species are at least partially responsible for microvascular reperfusion disorders.
Key words: antioxidants • cardiac arrest • cerebral blood flow • diffusion-weighted imaging • free radical scavengers • gene regulation • MRI • neuroprotection • outcomes • transgenic rats






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