Abstract
An ultrastructural and histological study was made to analyse the structural and cellular features of the pulmonary lesions produced in Wistar rats by intraperitoneal (i.p.) administration of cyclophosphamide (two i.p. doses of 150 mg CP/1 kg bw/1 ml PBS). Rats exposed to cyclophosphamide (CP) developed a condition whose morphological picture corresponded to endogenous lipid pneumonia and/or pulmonary alveolar proteinosis-like changes. Damage to the endothelium and neutrophil accumulation in lung vascular bed were found to be potential initiators of endogenous lipid pneumonia-type changes. The possibility of the evolution of the acute lung injury into endogenous lipid pneumonia-type changes and into alveolar proteinosis-like changes was demonstrated. The results of the study supplement the existing theories of pulmonary alveolar proteinosis pathogenesis.
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