Cerebrospinal fluid (CSF) lactic acidosis does not contribute to cerebral hyperemia in hemophilus influenzae type B (HIB) meningitis in rabbits

E. Gunnoe, I. D. Berkowitz, C. Newton

Research output: Contribution to journalArticlepeer-review

Abstract

Cerebral hyperemia characterizes the cerebrovascular circulation in acute Hib meningitis in rabbits. We tested the hypothesis that elevated CSF lactate concentration contributes to cerebral hyperemia by preventing CSF lactate accumulation with dichloroacetate (DCA) treatment. Intracisternal (1C) inoculation of either saline or Hib was performed in 4 groups of rabbits (n=8 each group) and groups received either intravenous (IV) saline or DCA: 1.1C saline and IV saline, 2.1C saline and 1C DCA, 3. IC Hib and IV saline, 4. 1C Hib and IV DCA. Cerebral blood flow (CBF - microspheres) was measured 18 hours later. DCA attenuated the rise in CSF lactate in the meningitis group. CBF increased significantly in the untreated meningitis group without significant changes in the cerebral perfusion pressure (CPP). The hyperemia was not reduced by DCA treatment. Group 1 Group 2 Group 3 Group 4 CSF lactate (m M/L) 1.1±0.l 2.2±0.4 6.3±0.4 2.3±0.1 CBF (ml/100g/min) 46±5 49±6 81±20 68±8 CPP(mmHg) 87±6 87±3 81 ±4 79±8 These data suggest that the rise in CSF lactate concentration in meningitis is not responsible for the associated cerebral hyperemia.

Original languageEnglish (US)
Pages (from-to)A588
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Fingerprint Dive into the research topics of 'Cerebrospinal fluid (CSF) lactic acidosis does not contribute to cerebral hyperemia in hemophilus influenzae type B (HIB) meningitis in rabbits'. Together they form a unique fingerprint.

Cite this