Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.


Journal article


FASEB Journal

Publication Date