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The effect of hypercapnia upon the sensitivity of the cerebral energy metabolism to low perfusion pressures was studied by decreasing the mean arterial blood pressure to 60 and 45 mm Hg, respectively, in rats maintained at arterial CO2 tension of 60–65 mm Hg. The hypercapnia gave rise to a moderate extra‐and intracellular acidosis. The cerebral venous Pco2 rose and remained above 50 mm Hg even in the hypotensive groups. In spite of this venous hyperoxia a reduction of the mean arterial blood pressure to 60 mm Hg gave rise to slight but consistant changes in the tissue concentrations of adenine nucleotides. At a pressure of 45 mm Hg there was a major derangement of the energy state of the tissue in 4 out of 6 animals. It is concluded that hypercapnic acidosis adversely affects the cerebral energy metabolism in hypotensive states, probably by inducing a flow pattern which leads to regional ischemia.
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Eklöf et al. (1973) studied this question.
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