Effects of hydrogen sulfide exposure on surface properties of lung surfactant

Abstract

Hydrogen sulfide is an irritant and chemical asphyxiant gas that exerts its primary toxic effects on the respiratory and neurological systems. Exposure to hydrogen sulfide above a threshold value of 200-300 ppm is characterized by the sudden onset of hemorrhagic pulmonary edema. The purpose of this study was to determine whether this response is associated with changes in the surface properties of pulmonary surfactant. Bronchoalveolar lavage fluid was retrieved from the lungs of Fischer 344 rats exposed to two concentrations of hydrogen sulfide or fresh air for 4 h. Surface tension-lowering properties were assayed using a captive bubble surface tensiometer. Lung injury was assessed by histopathology and measurements of total protein and lactate dehydrogenase activity in the lavagate. Marked abnormalities in surfactant activity were demonstrated in the lavagates from rats exposed to the highest concentration (300 ppm) of hydrogen sulfide. These involved the properties of adsorption to the air-water interface and surface tension lowering under quasi-static interfacial compression. Exposure to 200 ppm hydrogen sulfide had no effect on minimum surface tension despite a significant increase in protein and lactate dehydrogenase in the lavagate. This would suggest a threshold-type response for the inhibition of surfactant activity by hydrogen sulfide. In vitro studies using normal rat surfactant showed that the abnormalities in surfactant activity were due to inhibitors in the edema fluid and not to a direct effect of sulfide on surfactant. The pathophysiological consequences of increased alveolar surface tension after hydrogen sulfide exposure may need to be considered in the clinical setting.

Tracheal aspirate surface tension in babies with hyaline membrane disease: Effects of synthetic surfactant replacement

“…24 Upon first quasi-static compression, stable minimum surface tensions of about 1 mN/m are achieved with both protein containing surfactants 16,22,26 and synthetic surfactants, provided the film area compression is not limited to 50%. 27 Possible explanations for the relatively higher minimum surface tension measurements in our study include: 1) the phospholipid concentrations in samples from both the control and the EXOSURF group may have been too low (substantially below 50 g/mL of total phospholipid), 2) tracheal aspirate samples may have contained protein inhibitors, [28][29][30][31] or 3) the phospholipid composition in the tracheal aspirates might have been substantially different from that of alveolar surfactant.…”

Is a reduction in residual volume a sub-clinical manifestation of hydrogen sulfide intoxication?

“…Owens et al [1987] in a study of 69 patients noted this ®nding in a group of 11 subjects who had inhaled potentially toxic substances including ammonia, sulfur dioxide, and pesticides. Parra et al [1991] suggested the development of a mild ®brosis, with some decrease in lung volumes and gas transfer, subsequent to H 2 S inhalation while Green et al [1991] have demonstrated that exposure to H 2 S may adversely affect the properties of pulmonary surfactant.…”

Effect of Acidosis on Bilirubin-Lipid Extract Surfactant Interaction

“…Intracellu lar toxicity probably depends on the deposi tion of the diacid form in phospholipid struc tures [15].…”