Search

Background/Purpose:: Fetal tracheal occlusion (TO) causes accelerated lung growth. However, prolonged TO is associated with a decline in the type II cell number. Type II cell function after TO is unclear. Herein, the authors examine type II cell function after TO and the role of tracheal fluid. Methods:: Fetal lambs (term, 145 days) underwent TO at 122 days. Tracheal pressure was recorded daily. In one group of animals (TF; n = 6), lung fluid was aspirated, measured, and reinfused daily. In their respective twins, NS group, lung fluid was replaced milliliter per milliliter with normal saline (NS; n = 6). At death near term, lung weight was obtained, and tissues were processed for stereologic volumetry. Type II cells were quantitated using antisurfactant protein B immunohistochemistry. Surfactant protein B-mRNA expression was studied by Northern analysis. Wilcoxon signed rank test and single factor analysis of variance (ANOVA) were used for statistical analysis (P < .05 was significant). Results:: In both experimental groups, intratracheal pressure rose from 1.9 +/- 1.0 torr to 3.7 to 4.8 torr by day 1, and remained constant thereafter. Lung fluid volume increased from 11.9+/-4.2 on day 0 to 36.8 +/- 8.0 mL/kg in TF, and to 28.4 +/- 9.3 mL/kg in NS by day 1 (P < .05). At death, lung weight/body weight ratio was higher in TF (5.45% +/- 0.91%) than in NS (4.40% +/- 0.67%) or control (3.83% +/- 0.58%; P < .05). Type II numerical density was substantially reduced after TO: 57.7 +/- 12.8 x 10^6/mL (TF) and 45.0 +/- 25.9 x 10^6/mL (NS), versus 82.3 +/- 13.6 x 10^6/mL in controls. Ultrastructurally, remaining type II cells in TF were enlarged and engorged with lamellar bodies; in NS, they were smaller and contained fewer lamellar bodies. Surfactant protein B mRNA expression was significantly decreased in NS, but not in TF, compared with controls. Conclusions:: Type II cell function as well as overall lung growth are stimulated by TO. Lung growth after TO is therefore not unavoidably detrimental to type II cells. After isobaric saline exchange of lung fluid, type II cell function is severely inhibited, confirming the role of tracheal fluid composition in type II stimulating type II cell function.