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(Stroke. 1999;30:1679-1686.)
© 1999 American Heart Association, Inc.

Original Contributions

Effects of Moderate Hypothermia on Leukocyte- Endothelium Interaction in the Rat Pial Microvasculature After Transient Middle Cerebral Artery Occlusion

Mami Ishikawa, MD; Eliichi Sekizuka, MD; Shuzo Sato, MD; Noriyuki Yamaguchi, MD; Joji Inamasu, MD; Helmut Bertalanffy, MD Takeshi Kawase, MD

From the Departments of Neurosurgery (M.I.) and Internal Medicine (E.S.), Saitama National Hospital, Saitama, Japan; Department of Neurosurgery, School of Medicine, Keio University, Tokyo, Japan (S.S., N.Y., J.I., T.K.); and Department of Neurosurgery, Philipps University Hospital, Marburg, Germany (H.B.).

Correspondence to Mami Ishikawa, MD, Department of Neurosurgery, Philipps University Hospital, Baldingerstrasse, 35033 Marbury, Germany.

Background and Purpose—It has been demonstrated that moderate hypothermia attenuates brain damage, but the mechanism whereby this is achieved has not been clearly shown. Recently, the role of leukocytes as mediators of secondary brain damage after brain ischemia has been discussed. The aim of this study is to examine the effects of moderate hypothermia on leukocyte-endothelium interaction in the rat pial microvasculature after transient middle cerebral artery occlusion (MCAO).

Methods—Rhodamine 6G–labeled leukocytes in brain surface were visualized with intravital fluorescence videomicroscopy through a closed cranial window. We analyzed the number of leukocytes adhering to the venular and arteriolar endothelium before ischemic insult and up to 3 hours after reperfusion. Rats were divided into 4 experimental groups. Group I (n=6) consisted of sham-operated animals. Groups II (n=6) and III (n=6) received left MCAO for 1 hour under normothermia (36°C to 37°C, group II) and under moderate hypothermia (30°C to 32°C, group III). Group IV (n=4) received left common carotid artery occlusion for 1 hour under normothermia.

Results—The number of adhering leukocytes in venules in groups II and IV increased significantly (P<0.001) after reperfusion compared with the group I, but that in group III did not increase significantly (P>0.05). The number of adhering leukocytes in arterioles in group II increased significantly (P<0.01) compared with the other groups, although the adhering leukocytes were not as numerous as those seen in venules.

Conclusions—It is demonstrated that hypothermia attenuates adhering leukocytes in venules and arterioles after reperfusion of MCAO. The inhibition of the leukocyte function may be an important factor in the neuroprotective effect of hypothermia.

Editorial Comment

Costantino Iadecola, MD, Guest Editor

Laboratory of Cerebrovascular Biology and Stroke, Department of Neurology, University of Minnesota, Minneapolis, Minnesota