An investigation of the role of lactic acid production in the causation of metabolic acidosis resulting from raised intracranial pressure in rabbits.
Intracranial pressure (ICP) was acutely raised in anaesthetized rabbits by the injection of saline into the cisterna magna. The raised ICP was maintained at 200 mm Hg for 3 min after which it was allowed to return to baseline values. The profound metabolic acidosis produced (mean base deficit reaching 17.99 +/- SD 4.06 mmol/1 30 min after raised ICP) was found to be in part related to an increase in arterial blood lactate (from mean 7.04 +/- SD 3.26 mmol/l before raised ICP to mean 13.57 +/- SD 5.28 mmol/l 30 min after raised ICP). It would appear that systemic sympathetic nervous system discharge consequent upon raising ICP results in intense vasoconstriction and thus an increase in anaerobic metabolism and inorganic acid production.
D000138:Acidosis / Q000209:etiology*; D000818:Animals; D006863:Hydrogen-Ion Concentration; D007427:Intracranial Pressure; D007773:Lactates / Q000097:blood / Q000378:metabolism*; D019344:Lactic Acid; D011817:Rabbits; D014661:Vasoconstriction
D007773:Lactates; D019344:Lactic Acid