The influence of arterial hypoxia and unilateral carotid artery occlusion upon regional blood flow and metabolism in the rat brain.

The influence of marked arterial hypoxia combined with unilateral carotid artery clamping upon regional cortical metabolites and blood flow was studied in the rat brain. When the arterial Po, was reduced to about 20 mm Hg the hemisphere on the clamped side showed a marked lactic acidosis and a fall in phosphocreatine but the adenylate energy charge remained close to normal. In this hemisphere, the cortical blood flow increased about 4-fold. On the clamped side there was an excessive lactic acidosis and a marked fall in energy charge. However, since the levels of glucose, glucose-6-phosphate and pyruvate did not fall below normal, and since the regional blood flow was at least doubled, it is concluded that the derangement of the energy metabolism was due to cellular hypoxia, exaggerated by the relative ischemia induced by the carotid artery clamping. The biochemical lesion was most pronounced in the distribution territory of the middle cerebral artery that also showed the largest degree of relative ischemia. It is suggested that the pronounced lactic acidosis may contribute to the neuronal damage observed with this model of hypoxia and relative ischemia.