Question: 

Hydrogen sulfide is a gaseous signalling molecule which regulates a variety of physiological cell functions. However, high doses of hydrogen sulfide are toxic. Patients with hydrogen sulfide poisoning develop inter alia pulmonary edema. Since pulmonary fluid clearance is tightly associated with ion transport processes across lung epithelia, we hypothesized that there might be an impact of hydrogen sulfide on pulmonary transepithelial ion transport.

Methodology: 

Pulmonary transepithelial ion transport was measured as short-circuit current (I_SC) across human lung epithelial cells (H441) as well as native lung preparations (Xenopus laevis) by electrophysiological Ussing chamber experiments. For the application of hydrogen sulfide, the donor molecule NaHS was employed.

Results: 

The application of 300 mM NaHS led to a rapid decrease of the I_SC of H441 cells by 60 %. This effect was also observed on Xenopus lung preparations (50 % inhibition due to 1mM NaHS). There was no effect of NaHS on transepithelial resistance. The effect of NaHS was - in both models - sensitive to amiloride.

Conclusion: 

These data indicate that hydrogen sulfide impairs ion - and particularly amiloride-sensitive sodium transport - processes across the pulmonary epithelium. Although the precise targets for hydrogen sulfide remain to be investigated, these data suggest that the development of pulmonary edema as a result of hydrogen sulfide poisoning might be due to impaired edema resolution by transepithelial ion and consequently water transport.