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Mismatch Recovery of Regional Cerebral Blood Flow and Brain Temperature During Reperfusion After Prolonged Brain Ischemia in Gerbils

Tajima, Goro MD; Shiozaki, Tadahiko MD, PhD; Seiyama, Akitoshi PhD; Mohri, Tomoyoshi MD; Kajino, Kentaro MD; Nakae, Haruhiko MD; Tasaki, Osamu MD, PhD; Ogura, Hiroshi MD, PhD; Kuwagata, Yasuyuki MD, PhD; Tanaka, Hiroshi MD, PhD; Shimazu, Takeshi MD, PhD; Sugimoto, Hisashi MD, PhD

The Journal of Trauma: Injury, Infection, and Critical Care: January 2007 - Volume 62 - Issue 1 - p 36-43
doi: 10.1097/TA.0b013e31802dd73c
Original Articles

Background: Recovery of cerebral reperfusion after stroke or cardiac arrest can take a long time. We aimed to identify differences in the postischemic recovery of physiologic parameters between short and prolonged brain ischemia.

Methods: Eighteen Mongolian gerbils were assigned to one of three groups: 5-minute (G5), 15-minute (G15), or 30-minute (G30) ischemia. With the use of our original microspectroscopy system, global ischemic reperfusion was performed. We measured changes in regional cerebral blood flow (r-CBF), microvessel diameter, and brain temperature (BrT) simultaneously. We also monitored somatosensory evoked potentials (SEPs) to evaluate electrophysiologic response.

Results: Both G5 and G15 showed concurrent recovery of r-CBF and BrT with hyperemia and hyperthermia, respectively, 10 to 15 minutes after reperfusion. The increase in BrT was <1°C and recovered to baseline within 60 minutes after reperfusion. In G30, recovery of r-CBF was significantly delayed relative to that of BrT. The increase in BrT was >2°C, peaking approximately 15 minutes after reperfusion, and then maintained increases of >1°C for 120 minutes. SEPs in G5 and G15 showed concomitant recovery with that of r-CBF, whereas SEP recovery in G30 was delayed relative to that of r-CBF, eventually disappearing. All except one of the G30 gerbils died within 24 hours, but all in G5 and G15 survived.

Conclusions: These results suggest that mismatch recovery of r-CBF and BrT after prolonged ischemia initiates metabolic derangement in brain tissue, leading to the electrochemical dysfunction and mortality.

From the Departments of Traumatology and Acute Critical Medicine (G.T., T. Shiozaki, T.M., K.K., H.N., O.T., H.O., Y.K., H.T., T. Shiimazu, H.S.), and Physiology (A.S.), Osaka University Graduate School of Medicine, Osaka, Japan.

Submitted for publication August 14, 2006.

Accepted for publication November 2, 2006.

Supported by a grant from the Marine and Fire Insurance Association of Japan, Inc., a Research on Brain Science grant from the Ministry of Health, Labour and Welfare of Japan (no. 15131001), and a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (no. 15390545).

Presented at the 65th Annual Meeting of the American Association for the Surgery of Trauma, September 28–30, 2006, New Orleans, Louisiana.

Address for reprints: Goro Tajima, MD, Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, 2-15, Yamadaoka, Suita, Osaka 565-0871, Japan; e-mail:

© 2007 Lippincott Williams & Wilkins, Inc.