Abstract

To determine the suitability of plasma hypoxanthine as a marker of tissue hypoxia, we studied the relationship of arterial plasma hypoxanthine and blood lactate concentrations to the cumulative O2 deficit during hypoxemia and low cardiac output (hypoxic and stagnant hypoxia, respectively). Eight intact, chronically catheterized lambs were studied using ketamine sedation. Comparable reductions in O2 transport and consumption were produced with each form of hypoxia. Lactate was linearly related to O2 deficit during both forms of hypoxia, although the slope of the regression was greater for low cardiac output (0.049) than hypoxemia (0.032). Hypoxanthine was linearly related to cumulative O2 deficit only during low cardiac output. During hypoxemia, hypoxanthine concentration initially increased but plateaued with further increases in O2 deficit. The discrepancy in response of hypoxanthine was most likely caused by differences in the rate of elimination between stagnant and hypoxic hypoxia. We concluded that plasma hypoxanthine concentration was not a reliable marker for tissue hypoxia because it differed with the cause of O2 deprivation and did not necessarily reflect the severity of O2 deprivation.

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