The relationship between arterial po2 and cerebral blood flow in hypoxic hypoxia

Abstract

The relationship between arterial oxygen tension (PaO2) and cerebral blood flow (CBF) in hypoxic hypoxia was studied in artificially ventilated and normocapnic rats. Changes in CBF were evaluated from arteriovenous differences in oxygen content after 2, 5, 15 and 30 min exposure to PaO2 85, 75, 55, 45, 35, and 25 mm Hg. In separate experiments the PaO2 was decreased to 25 mm Hg for 1, 2, 5, 15 and 30 min in animals in which PaCO2 was allowed to fall by 5-10 mm Hg. There was a small, gradual increase in CBF when PaO2 was lowered in steps from 130 to 55 mm Hg, and a more pronounced increase at PO2 values below 50 mm Hg. At PaO2 25 mm Hg CBF increased to values of 500% of normal. Significant increased in CBF were recorded at PaO2 values of 85 and 75 mm Hg in spite of the fact that previous studies have failed to record an elevated tissue lactate content at these po2 levels, and in spite of an unchanged cerebral venous PO2. When the PaO2 was reduced to 25 mm Hg CBF increased markedly already at 1 and 2 min, and this increase in CBF occurred even if PaCO2 was allowed to fall by 5-10 mm Hg. Previous results have shown that in such short periods enough lactic acid is not formed to induce a net tissue acidosis. The results thus give no support to the hypothesis that cerebral hyperemia in hypoxia is coupled to accumulation of lactic acid in the tissue.