Stroke, Vol 21, 614-617, Copyright © 1990 by American Heart Association
KU Frerichs, PJ Lindsberg, JM Hallenbeck and GZ Feuerstein
Increased cerebral lactate levels are a well-known aspect of the sequelae
of the metabolic derangements that follow cerebral ischemia. A new
technique has recently become available to sample cerebral venous blood
from the superior sagittal sinus on a long-term basis in conscious rats. We
report the applicability of this method to assess serial biochemical
responses to brain injury. Serum samples were obtained from the superior
sagittal sinus, the common carotid artery, and the external jugular vein of
nine anesthetized rats before and up to 7 days after 10 minutes of
forebrain ischemia was produced by carotid occlusion and hypovolemic
hypotension (mean arterial blood pressure 50 +/- 4 mm Hg). The cerebral
venous-arterial difference in serum lactate concentration was increased for
up to 3 hours after ischemia, while there was no significant change in the
difference in serum lactate concentrations in the common carotid artery and
the external jugular vein. This indicates an elevated output of lactate
from brain tissue to blood, detectable only in the superior sagittal sinus,
which underlines the usefulness of the technique. We observed a persistent
elevation in brain lactate production after virtually complete recovery
from the acute insult.
ARTICLES
Increased cerebral lactate output to cerebral venous blood after forebrain ischemia in rats
Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814.