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© 1989 Oxford University Press

research-article

Peracute Toxic Effects of Inhaled Hydrogen Sulfide and Injected Sodium Hydrosulfide on the Lungs of Rats

ALFONSO LOPEZ*,1, MICHAEL G. PRIOR*, R. J. REIFFENSTEIN{dagger},2 and LORNE R. GOODWIN{ddagger}

*Animal Sciences Wing Wing, Alberta Environmental Centre. Bag 4000, Vegrville. Alberta, Canada T0B 4L0. {dagger}Department of Pharmacology, University ofAlberta Edmonton. Alberta, Canada T6G 2H7 {ddagger}Chemistry Wing Alberta Environmental Centre. Bag 4000, Vegreville. Alberta, Canada T0B 4L0.

Received May 4, 1988; accepted July 28, 1988

Peracute Toxic Effects of Inhaled Hydrogen Sulfide and Injected Sodium Hydrosulfide on the Lungs of Rats. LOPEZ, A., PRIOR, M. G., REIFFENSEIN, R. J., AND GOODWIN, L. R. (1989). Fundam Appl Toxicol. 12, 367–373. This study was designed to test whether intraperitoneally injected sodium hydrosulfide (NaHS) would mimic the pulmonary alterations induced by lethal peracute exposure to an atmosphere containing hydrogen sulfide. Groups of five Sprague- Dawley rats were exposed to an atmosphere of either 2317.6 ± 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were injected intraperitoneally with a solution containing 30 mg kg-1 sodium hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of the air and saline groups were killed by cervical dislocation. All rats exposed to H2S or injected with NaHS died within 3 min; however, only rats exposed to H2S showed severe respiratory distress in the agonic phase preceding death. In addition, rats in the H2S group had a notable discharge of serous fluid from the mouth and nostrils. At necropsy, all rats in the H2S group had gross and histologic evidence of pulmonary edema characterized by massive extravasation of eosinophilic fluid into the bronchcalveolar space. In contrast the lungs of rats injected with NaHS or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of H2S in the lungs cannot be reproduced by injection of NaHS. The severity of lung edema induced by a peracute exposure to H2 was extensive enough to account for death.


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