OBJECTIVETo study the effect of captopril on the histopathology and bronchoalveolar lavage fluid (BALF) in neonatal rats exposed to hyperoxia.

METHODSForty term neonatal Wistar rats were randomly assigned into Air control, Model, Normal saline control and Captopril-treated groups (n=10 each). The Air control group was exposed to air (FiO2=0.21). The remaining three groups were continuously exposed to hyperoxia (FiO2=0.90) . During exposure the Captopril-treated group received intragastric captopril (60 mg/kg daily) and the Normal saline control group was administered with normal saline. The Model group had no treatment. At the 14th and 21st days of exposure, the subjects were sacrificed. The lung coefficient and the protein contents and inflammatory cells in BALF were determined. The changes of lung histomorphology were observed.

RESULTSThe lung coefficient and the protein contents, the total number of cells and the percentage of neutrophils, lymphocytes and eosinophils in BAFL increased significantly in the Model and Normal saline control groups on the 14th and 21st days of exposure compared with those of the Air control group. Captopril treatment significantly reduced the lung coefficient and the protein contents, the total number of cells and the percentage of neutrophils and eosinophils in BALF. On the 14th day the lung coefficient decreased from 9.72 +/- 0.67 mg/g to 8.63 +/- 0.35 mg/g (P < 0.05); the protein contents in BALF from 0.619 +/- 0.023 g/L to 0.486 +/- 0.027 g/L (P < 0.05); and the total number of cells in BALF from (80.57 +/- 9.28)x10(4)/mL to (48.62 +/- 1.53)x10(4)/mL (P < 0.01) compared with the Model group. On the 21st day the lung coefficient decreased from 10.67 +/- 0.87 mg/g to 8.76 +/- 0.89 mg/g (P < 0.05); the protein contents in BALF from 0.978 +/- 0.012 g/L to 0.759 +/- 0.042 g/L (P < 0.05); and the total number of cells in BALF from (92.86 +/- 10.32) x10(4)/mL to (35.52 +/- 3.89) x10(4)/mL (P < 0.05) compared with the Model group. There were however significant differences in these results between the Captopril-treated and Air control groups. The histopathological examination demonstrated different degrees of alveolitis, broaden interstitium and reduced alveolar quantity in the Model and Normal saline control groups. The pathological changes were markedly alleviated after captopril treatment.

CONCLUSIONCaptopril may have protective effects on lung injury induced by hyperoxia.