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Fifty percent of the ascorbic acid content of sliced rat lung was released from the tissue to the media within a few minutes by either washing or incubating the slices with Krebs-phosphate solution. Measurement of the lactate dehydrogenase and potassium content of the medium after incubating lung slices for 5 min showed that about 20% of the cells were damaged by slicing. Sephadex chromatography of tissue extracts prepared from washed lung slices showed that none of the ascorbic acid in these slices were bound to protein. Also, metabolic poisons were shown to deplete the ascorbic acid content of washed lung slices. Approx. 57% of the lung ascorbic acid of guinea pigs that had been supplemented with ascorbic acid and 78% of the lung ascorbic acid of ascorbic acid-deficient guinea pigs were found in the medium when lung slices from these animals were incubated with Krebs-phosphate solution. These results were taken to indicate the presence of an extracellular pool of ascorbic acid in lung which is maintained even during scurvy.

Mice were exposed to concentrations of 20, 40 and 200 ppm ozone in air for 30 min. Ozone exposure decreased lung ascorbic acid levels and increased lung weight by up to 50% in a dose related manner. On incubation in Krebs-phosphate solution, lung slices from mice exposed to 200 ppm ozone released a smaller fraction of their content of ascorbic acid into the medium than did lung slices from control mice, suggesting that there was a preferential loss of extracellular ascorbic acid during oxone exposure. These results are consistent with the proposed function of ascorbic acid as an extracellular antioxidant in lungs.

Rat lungs were perfused by recycling Krebs-bicarbonate solution in an apparatus which allowed negative pressure ventilation of the lungs. After addition of either reduced or oxidized ascorbic acid to the perfusion fluid serial samples were taken over 60 min and assayed for ascorbic acid. At the end of perfusion, lungs were assayed for ascorbic acid. The results show that reduced ascorbic acid was taken up by the lung and concentrated in the tissue. No appreciable transport of oxidized ascorbic acid was measured.

Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated this effect. Given alone, hexamethonium caused both loss of ascorbic acid and pulmonary edema. The results show that although endogenous catecholamines can potentiate the pulmonary edema produced by either adrenaline or noradrenaline, they play no specific role in the ascorbic acid loss. The evidence suggests that lung ascorbic acid levels are decreased following the development of pulmonary edema, irrespective of how it was caused.