Increased cerebral lactate output to cerebral venous blood after forebrain ischemia in rats.

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.