Glucose utilization by edematous rat lungs

Abstract

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.