Abstract
Cerebral ATP, lactate, and pyruvate concentrations were measured bilaterally in 21 squirrel monkeys 2 hours after occlusion of the right middle cerebral artery (MCA). All animals were mechanically hyperventilated beginning 30 minutes after MCA occlusion. Effects of addition of various concentrations of CO2 to inspired gases were studied in three groups (seven animals in each): 1) hypocapnic (Paco2 = 20 mm Hg); 2) normocapnic (Paco2 = 40 mm Hg); 3) hypercapnie (Paco2 = 60 mm Hg). Results in these animals were compared with those obtained in six monkeys breathing room air spontaneously during the 2-hour occlusion period (Paco2 ≈ 30 mm Hg). In the hypocapnie animals, cerebral ATP was significantly less and cerebral lactate significantly greater than corresponding values in the hypercapnie and spontancously breathing monkeys. We conclude that hypocapnia induced by mechanical hyperventilation does not improve, but rather aggravates, the cerebral metabolic effects of ischemia induced by MCA occlusion. Three possible mechanisms are suggested to explain the deleterious effects of hypocapnia: the effect of pH on glycolytic activity, the direct effect of CO2 on cerebral blood flow, and the systemic effects of hypocapnia and mechanical hyperventilation.
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