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Research Article Free access | 10.1172/JCI114475

Loss of cerebrovascular autoregulation in experimental meningitis in rabbits.

J H Tureen, R J Dworkin, S L Kennedy, M Sachdeva, and M A Sande

Department of Pediatrics, University of California, San Francisco General Hospital 94110.

Find articles by Tureen, J. in: JCI | PubMed | Google Scholar

Department of Pediatrics, University of California, San Francisco General Hospital 94110.

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Department of Pediatrics, University of California, San Francisco General Hospital 94110.

Find articles by Kennedy, S. in: JCI | PubMed | Google Scholar

Department of Pediatrics, University of California, San Francisco General Hospital 94110.

Find articles by Sachdeva, M. in: JCI | PubMed | Google Scholar

Department of Pediatrics, University of California, San Francisco General Hospital 94110.

Find articles by Sande, M. in: JCI | PubMed | Google Scholar

Published February 1, 1990 - More info

Published in Volume 85, Issue 2 on February 1, 1990
J Clin Invest. 1990;85(2):577–581. https://doi.org/10.1172/JCI114475.
© 1990 The American Society for Clinical Investigation
Published February 1, 1990 - Version history
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Abstract

The present study was designed to determine whether cerebrovascular autoregulation is intact in experimental meningitis and to examine the relationship between fluctuations in cerebral blood flow (CBF) and increased intracranial pressure (ICP). Measurements of CBF were determined by the radionuclide microsphere technique in rabbits with experimental Streptococcus pneumoniae meningitis with simultaneous ICP monitoring via an implanted epidural catheter. CBF and ICP measurements were determined at baseline and when mean arterial blood pressure (MABP) was artificially manipulated by either pharmacologic or mechanical means. CBF was pressure passive with MABP through a range of 30-120 torr, and ICP directly correlated with CBF. These findings indicate that autoregulation of the cerebral circulation is lost during bacterial meningitis, resulting in a critical dependency of cerebral perfusion on systemic blood pressure, and that the parallel changes in ICP and in CBF suggest that fluctuations in CBF may influence intracranial hypertension in this disease.

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