The effect of carbon dioxide on cerebral blood flow and cerebral metabolism in dogs.
In 11 normally oxygenated, normotensive mongrel dogs, blood flow and oxidative metabolism of the brain was studied during normocapnia and during respiratory alkalosis and respiratory acidosis. During respiratory alkalosis (mean PaCO2 17.8 mm Hg) CBF decreased significantly from 61.0 to 33.9 ml/100 g/min (44%) while arteriovenous-substrate differences increased and the rates of oxygen and glucose metabolism remained constant. Cerebral venous-arterial difference of lactate was increased significantly as compared with the resting state. During hypercapnia CBF increased significantly from 61.0 (resting state) to 115.7 ml/100 g/min (89%) (mean PaCO2 64.7 mm Hg). The arteriovenous-substrate differences decreased while the cerebral metabolic rates remained constant. The data show that the relationship between PaCO2 and CBF in the range 20-65 mm Hg PaCO2 is expressed by a linear relationship: y = 2.88 + 1.69x; in this range, the oxidative metabolism of the brain is unchanged and the increased cerebral lactate production in respiratory alkalosis is not necessarily linked to tissue hypoxia.
D000142:Acidosis, Respiratory / Q000503:physiopathology; D000472:Alkalosis, Respiratory / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood / Q000494:pharmacology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004285:Dogs; D005947:Glucose / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D010100:Oxygen / Q000097:blood
D007773:Lactates; D002245:Carbon Dioxide; D005947:Glucose; D010100:Oxygen