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(Stroke. 1999;30:2623.)
© 1999 American Heart Association, Inc.

Original Contributions

Distributions of Local Oxygen Saturation and Its Response to Changes of Mean Arterial Blood Pressure in the Cerebral Cortex Adjacent to Arteriovenous Malformations

Presented in part at the Proceedings of the Second Conference on Cerebral Oxygenation held in Würzburg, Germany, September 1997, and published in abstract form in Neurological Research 1998;20(suppl 1).

Bernhard Meyer, MD; Carlo Schaller, MD; Christian Frenkel, MD; Bernd Ebeling, MD Johannes Schramm, MD, PhD

From the Departments of Neurosurgery (B.M., C.S., J.S.) and Anesthesiology (C.F., B.E.), University of Bonn (Germany).

Correspondence to Bernhard Meyer, MD, Department of Neurosurgery, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany. E-mail bmey{at}mailer.meb.uni-bonn.de

Background and Purpose—To test the hypothesis that neither "steal" as cortical ischemia caused by reduced perfusion pressure nor "breakthrough" on the grounds of loss of pressure autoregulation exist in brain tissue surrounding arteriovenous malformations (AVMs), we established patterns of cortical oxygen saturation (SO₂) adjacent to AVMs and its behavior after alterations of mean arterial blood pressure.

Methods—With a microspectrophotometer, SO₂ was scanned in the cortex around AVMs of 44 patients before and after resection and in that of a non-AVM group (n=42) before transsylvian dissection. Autoregulation was evaluated by linear regression analysis after elevation of mean arterial blood pressure (5 µg/min IV noradrenaline). SO₂ values were calculated as medians, percentage of critical values (<25% SO₂), and coefficients of variance (approximate heterogeneity of SO₂ distributions). All values are given as mean±SD.

Results—Forty patients with AVM had an uneventful postoperative course (group A). Four hyperemic complications ("breakthrough") occurred (group B). Autoregulation was tested intact in all groups at all times. Preoperative SO₂ distributions in groups A and C (non-AVMs) were identical. In group B, significantly (P<0.05) lower medians (group A, 52.9±16.3%; group B, 44.2±17.1%; group C, 51.9±11.5% SO₂), more critical values (group A, 6.5±5.1%; group B, 14.7±11.1%; group C, 7.1±4.9%), and heterogeneous SO₂ distributions (group A, 20.2±12.7%; group B, 27.9±12.4%; group C, 26.8±10.9%) were seen. Increase of median values was significantly higher in group B (76.3±10.4% SO₂) than in group A (65.9±13.4% SO₂) after resection.

Conclusions—Severely hypoxic areas are uncommon in the cortex adjacent to AVMs and occur predominantly in patients prone to hyperemic complications. Reduced perfusion pressure is compensated in most cases, and moderate hyperemia prevails after excision. Reperfusion into unprotected capillaries of severely hypoxic cortical areas results in "breakthrough," for which vasoparalysis appears not to be the underlying mechanism.

Key Words: autoregulation • cerebral arteriovenous malformations • cerebrovascular circulation • oxygen

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