Correlation of Changes in Pulmonary Surfactant Phospholipids with Compliance in Bleomycin-Induced Pulmonary Fibrosis in the Rat

Abstract

Qualitative and quantitative analysis was performed on phospholipids isolated from bronchoalveolar lavage fluid during the development of pulmonary fibrosis in the rat. A single transtracheal injection of 2.0 units of bleomycin was administered to rats to induce lung injury. Animals were killed at 0, 3, 7, 14, 30, and 120 days after bleomycin treatment. Total lipid phosphorus in BAL from animals given bleomycin increased from 1.6 mumol/lung in normal animals to 3.2 mumol/lung at 14 and 30 days. The increase in phospholipids was primarily in phosphatidylcholine with minor increases in phosphatidylinositol and phosphatidylethanolamine. These quantitative changes were accompanied by qualitative changes that included an increase in the percentage of total phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylinositol. In contrast, the percentage of phosphatidylglycerol was significantly reduced. Plasma phospholipid analysis indicated that these alterations were not due to plasma contamination. The functional significance of the phospholipid changes was assessed by comparing air- and saline-filled compliance measurements at similar times after bleomycin. Abnormal compliance measurements were observed at 3, 7, and 14 days after bleomycin. At 3 and 7 days the predominant compliance defect was at the air-liquid interface; however, at 14 days, when phospholipids were significantly elevated, the defect was primarily due to tissue components.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung volume quantified by MRI reflects extracellular-matrix deposition and altered pulmonary function in bleomycin models of fibrosis: effects of SOM230

“…These changes in lung structure lead to a severe impairment of lung function related to a decreased elasticity. Indeed, increased lung elastance as well as decreased compliance (the reciprocal of elastance) have been shown in humans (19,26,38) and in small rodent pulmonary fibrosis models (1,7,12,15,30,53,57,58). Moreover, changes in tidal volume and breathing cycle times have been shown in a mouse fibrosis model (33).…”

Feitai Attenuates Bleomycin-Induced Pulmonary Fibrosis in Rats

“…Lesions observed in the early stages of lung damage induced by BLM resemble chronic human fibrotic lung disease, both histologically and physiologically. [12][13][14][15][16][17][18][19][20] Interventions designed to limit the consequences of the inflammatory response [such as corticosteroids, anti-tumor necrosis factor (TNF)-a antibody, and anti-transforming growth factor (TGF)-b antibody] and to protect the lung from oxidant damage (such as Ginkgo biloba extract, 8) metalloporphyrin, 9) and N-acetylcysteine 10) ) are effective in suppressing BLM-induced pulmonary fibrosis. These findings suggest that inhibition of lung inflammation and lipid peroxidation may be employed as therapeutic strategies for pulmonary fibrosis in the clinic.…”

Composition of Lung Lavage in Pulmonary Alveolar Microlithiasis

“…Pulmonary disease often decreases many surfactant phospholipids, e.g. PG is lowered in adult respi ratory distress syndrome [32], silicosis [33], idiopathic pul monary fibrosis [12,34], Pneumocystis carinii pneumonia in rats [35], bleomycin penumonitis in rats [36] and acute alveolar injury resulting from N-nitroso-N-methylurethane exposure [35].Yet, raised levels of PG were found in the patient with PAM. No other lavage results have been pub lished from any species (baboon, monkey, dog, rat, hamster or rabbit) with PG concentrations more than half those found in our patient.…”