Abstract

Rats convulsed by hyperbaric oxygen (OHP) or by pentylenetetrazol (PTZ) suffer consolidative lung damage. This effect and its moderation by pretreatment of the animals with protective compounds were quantitated by measuring lung weight and lung non-protein sulfhydryl (NPSH) content; liver NPSH content was also measured. Changes in lung weight were also examined in mice, guinea pigs, and rabbits treated with these two agents. Rats and mice convulsed by either OHP or PTZ suffered a similar degree of lung damage. This effect was absent when exposures did not lead to onset of convulsive seizures. In contrast, guinea pigs and rabbits convulsed by OHP for similar times sustained considerably less lung damage. PTZ-induced convulsions in these two species did not lead to significant increases in lung weight. Rats convulsed with OHP or PTZ had an identical loss of NPSH (44 %) from lung but much less loss (25 %) from liver. The liver NPSH loss was duplicated by non-convulsive OHP treatment, while lung NPSH content was relatively unaffected by such exposures. Starvation for 18 hr depleted liver NPSH levels but led to no greater loss of this component under OHP. Lung weight increases and lung NPSH loss due to PTZ were prevented by prior administration of compounds, (e.g. 5-hydroxytryptamine), known to prevent effects of OHP. The experimental data were contrasted with the results of clinical experience with human patients. The conclusion was reached that the gross aspects of OHP-induced lung damage in animals are probably attributable to some mechanism other than direct oxidative attack upon pulmonary structures.

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