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Angiotensin II and its role in fat embolism‐induced lung pathology
Author(s) -
Abbas Fizza,
Herndon Betty,
Quinn Tim,
Likhitsup Alisa,
Salzman Gary,
Molteni Agostino
Publication year - 2013
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.27.1_supplement.lb446
Subject(s) - losartan , angiotensin ii , captopril , medicine , histology , endocrinology , lung , triolein , pathology , chemistry , receptor , blood pressure , biochemistry , lipase , enzyme
Fat embolism (FE) after bone fractures increases pulmonary pathology. Our data suggests that lung damage in rats is less severe when angiotensin blocking drugs including captopril or losartan are given. Preliminary to my study, fat embolism was induced by i.v. injection of 0.2 ml triolein into 60 rats. Some animals received 50 mg/kg captopril i.p. or 10 mg/kg losartan i.p. one hour after triolein. Lungs were fixed for histology, or frozen for later study at 24–96 hr. Angiotensin peptides, detected by histochemistry, were increased by triolein‐induced FE compared to saline controls, and both captopril and losartan reduced the histochemical inflammation and fibrosis. Angiotensin II (A II) appeared to be mediating FE ‐induced pathology. To determine relationship of histology to tissue AII, lungs of 60 rats were homogenized into 500 μL protein buffer with protease inhibitor. Peptides were purified on micro C‐18 columns then tested by ELISA for AII. The angiotensin peptide present in lungs of rats with fat embolism syndrome increased from 24 (0.049) to 96 hr (0.062). The drugs produced significant increases in AII in the lungs (0.14 – 0.17 at 48 hr; p=0.001). Both ACE inhibitor captopril and AT1 blocker losartan partly improved pulmonary histology in animals given fat embolism in vivo. Comparison of pulmonary histology and A II peptide levels in the lungs continues with more mechanistic study. Funding: Gelmacher Foundation