To the Editor: The article by O'Connor et al.1 suggests that depletion of cellular stores of ATP may be responsible for a decrease in left ventricular stroke work. Although we find this explanation attractive, it seems to us that an alternate mechanism can be postulated. A decreased 2,3-diphosphoglycerate level (2,3-DPG) (secondary to hypophosphatemia)2 would result in a leftward shift of the oxygen-hemoglobin dissociation curve and a decrease in peripheral oxygen release. By replacing phosphorus, the reversal of myocardial depression reported by O'Connor was perhaps due to increased oxygen release to the myocardium secondary to repletion of 2,3-DPG. This hypothesis would.
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