Edema was produced in the isolated perfused rat lung by raising left atrial pressure. Eleven control lungs consumed 18±3.9 µmoles glucose/lung · hr−1 and released 17.1±4.2 µmoles lactate/lung · hr−1. During pulmonary edema in 13 isolated perfused lungs, glucose consumption was 35.5±8.8 µmoles/lung · hr−1 (P<.05) and lactate production was 37±5.9 µmoles/lung · hr−1 (P<.05). Separation of radiolabeled glucose and lactate indicated that all lactate was derived from glucose in control and edematous lungs. We found no important difference in14CO2 production from 1-14C, 6-14C, or14C(U)-glucose. Tissue slices of lungs made edematous in vivo had differences in glucose consumption and lactate production which were similar to those observed in the isolated lungs. Oxygen consumption by 1 mm thick lung slices was 224±9.7 µl O2/mg DNA · hr−1 in control and 218±18 µl O2/mg DNA · hr−1 in edematous lungs. When dinitrophenol was added to the medium, the QO2 was greater in the control than in the edematous lung slices (391±22 µl O2/mg DNA · hr−1 control vs. 334±33 µl O2/mg DNA · hr−1 edema,P<.05). We concluded that pulmonary edema in the isolated rat lung is accompanied by: 1) greater glucose consumption; 2) greater lactate production; 3) no important difference in14CO2 production from pentose pathway or tricarboxylic cycle activity; and 4) lower response of edematous tissue slices to dinitrophenol stimulation.
Key wordsPulmonary edema Lung oxygen consumption Lung glucose consumption Lung lactate production
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