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J Thorac Cardiovasc Surg 2001;122:734-740
© 2001 The American Association for Thoracic Surgery


Cardiopulmonary Support and Physiology

Experimental study on the effect of antegrade cerebral perfusion on brains with old cerebral infarction

Naoki Washiyama, MDa, Teruhisa Kazui, MDa, Makoto Takinami, MDa, Katsushi Yamashita, MDa, Syouji Fujita, MDa, Hitoshi Terada, MDa, Kazuchika Suzuki, MDa, Bashar A. H. Muhammad, MBBSa, Michio Fujie, MSb, Seiji Yamamoto, MDc

From the First Department of Surgery,a Research Equipment Center,b and Photon Medical Research Center,c Hamamatsu University School of Medicine, Hamamatsu, Japan.

This work was supported by a Grant-in-Aid for Scientific Research (C) in Japan Society for the Promotion of Science.

Received for publication Nov 28, 2000. Revisions requested Jan 16, 2001; revisions received Feb 12, 2001. Accepted for publication Feb 28, 2001. Address for reprints: Naoki Washiyama, MD, First Department of Surgery, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu 431-3192, Japan (E-mail: nwashi{at}akiha.hama-med.ac.jp).

Objective: Patients with old cerebral infarction who undergo aortic arch operations are susceptible to postoperative neurologic dysfunction. To verify such susceptibility, we performed this experimental study.
Methods: A cerebral infarct model was created in mongrel dogs by means of injection of cylindrical silicone embolus through the internal carotid artery. The dogs that had obvious neurologic deficits 1 day later and survived for 4 weeks or more were included in the cerebral infarct model. One month after cerebral infarction was induced, deep hypothermia and selective cerebral perfusion were used in 14 mongrel dogs (infarct group, n = 7; control group, n = 7). During this procedure, serum glutamate concentration and venous-arterial lactate difference were measured. Histopathologic study of the brain was also performed.
Results: Changes in venous-arterial lactate difference in both groups were almost similar, except in the rewarming phase. At 32°C during rewarming, the venous-arterial lactate difference in the infarct group was significantly higher than that in the control group (P = .006). Although precooling concentrations of serum glutamate were similar in both groups, the values in the infarct group at the end of rewarming were significantly higher than those in the control group (P = .046). On histologic examination, the presence of old cerebral infarction with gliosis was confirmed in the infarct group, but neither new cerebral infarction nor destruction of the bloodbrain barrier was found.
Conclusion: We observed an accelerated anaerobic metabolism and an increased extracellular glutamate release in the infarct group. The brain with old cerebral infarction is more susceptible to ischemia during arch operation than noninfarcted brain.




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