Abstract

The alveolar epithelium (AE) of fetal lungs actively transports Cl− into the alveolar lumen, resulting in a high concentration of Cl− in fetal lung fluid. REcently, we found that in the aqueous subphase (AS) of mature alveoli the Cl− concentration is equal to that in serum, consistent with little or no active transport of Cl− by the resting AE. If a Cl− pump exists in mature AE, then drugs that stimulate or decrease active Cl− transport in other tissues might alter the concentration of Cl− in the AS. To test this hypothesis, we measured the concentration of Cl− in the AS of anesthetized rabbits before and after intravenous terbutaline (0.3 mg/kg), a drug that stimulates active Cl− transport in other types of respiratory epithelia. The measurements were made by puncturing alveoli visible through the pleura with a Cl− selective microelectrode. Baseline Cl− = 98 ± 5 meq/L (mean ± SD, n = 5). The Cl− increased to 116 ± 4 (n = 5) within 30 to 40 min after the terbutaline, a significant change (p<0.001). Three rabbits received intravenous furosemide (5 mg/kg), known to block Cl− transport in other tissues, 60 min after the terbutaline. In those rabbits the baseline Cl− = 94 ± meq/L, 30 to 60 min after terbutaline Cl− = 114 ± 3, and 20 min after furosemide Cl− = 101 ± 5. Furosemide without prior terbutaline did not change AS Cl− (n = 5). BAsed on these data, the Cl− pump found in the AE of fetal lambs is much less active or inactive in mature lungs of rabbits, but it can be stimulated and blocked by appropriate drugs.

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