HYPERBARIC HYPEROXIA EXAGGERATES RESPIRATORY MEMBRANE DEFECTS IN THE COPPER-DEFICIENT RAT LUNG

Scanning (SEM) and transmission electron microscopy (TEM) were used to examine the effect of dietary copper deficiency and hyperbaric hypero xia, alone and in combination, on lung structure. Male, weanling Sprag ue-Dawley rats were fed a copper-deficient (CuD, 0.2 mug/g) or copper- adequate diet (CuA, 5.1 mug/g). After 35-41 d on their respective diet s, rats from each group were placed inside a pressure vessel kept at 2 7-degrees-C under one of two pressure protocols. Air controls were mai ntained at 1 atm for 75 min. Rats exposed to oxygen were maintained at 1 atm of air plus 3 atm of oxygen for 1 h and then decompressed for 1 5 min. Under SEM, none of the treated lungs (CuD, CuA-O2 exposed, or C uD-O2 exposed) showed abnormal lung morphology from the conducting bro nchioles down to the alveoli. Copper-deficient red blood cells were ab normally shaped. Under TEM, CuA-O2-exposed lungs showed thicker respir atory membranes, especially basement membranes and endothelial cells, and alveolar Type II cells having more than the usual number of surfac tant vacuoles. CuD lungs also showed thicker endothelial and basement membrane components of the respiratory membrane, but normal looking Ty pe II cells. CuD-O2-exposed lungs showed greatly thickened respiratory membranes and severe disruption of both endothelium and basement memb rane and, judging by the increased number of nuclei per field, an incr ease in the number of both Type I and Type II cells. We conclude that copper deficiency enhances the damage caused by O2 toxicity, an effect that may be caused by reduced antioxidant status.