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The Role of Mast Cells in a Fat Embolism Model
Author(s) -
Vijaypura Charmi,
Poisner Alan,
Lankachandra Kamani,
Dim Daniel,
Herndon Betty,
Rawls Jennifer,
McIff Terrence,
Adler Federico,
Molteni Agostino
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb418
Subject(s) - medicine , triolein , lung , mast cell , losartan , fibrosis , inflammation , captopril , pathology , degranulation , fat embolism , endocrinology , angiotensin ii , immunology , receptor , chemistry , biochemistry , lipase , blood pressure , enzyme
Mast cells are found in many cases of bronchial and pulmonary damage. Fat embolism, an event consequent to long bone fractures, often precedes pulmonary damage. This study reports mast cell response in a fat embolism model of lung damage in the rat. Pure triolein (0.2 mL) or saline (controls) were injected (i.v.)into 44 rats, sacrificed at 24, 48, 96 hr and 3 or 6 weeks. Five rats received captopril (50 mg/kg), losartan (10 mg/kg) or both drugs. Lungs were formalin fixed and stained for mast cells. Three pathologists independently counted peribronchial and subpleural areas for stained cells. Triolein treated rats showed severe inflammation of bronchi and lungs, pulmonary fibrosis, vasculitis with marked occlusion of arteries, effects which peaked at 96 hr with partial recovery at 3 and 6 weeks. Fat was present, reduced in amount, up to 6 weeks. Captopril, losartan or their combination produced reduced inflammation and greater lumen patency. Mast cells occurred in both triolein treated rats and controls in similar numbers. Combination treatment with the two drugs resulted in a significant increase of bronchial mast cells, p=0.001, ANOVA and post‐tests. Renin secretion has been reported in pulmonary mast cells. The mast cell response to drugs regulating the renin angiotensin system suggests a need for study of this system to clarify protection mechanisms in fat‐induced lung damage.