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Mast Cell Numbers In Rat Livers In An Acute Model Of Fat Embolism Are Reduced By Losartan But Not By Captopril
Author(s) -
Siddiqi Ahsan,
Hamdan Hana,
Siddiqi Saba,
Pour Mohammad,
Randall Zachary,
Leupold Brad,
Arif Dauod,
Poisner Alan,
Hamidpour Soheila,
Molteni Agostino
Publication year - 2018
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.2018.32.1_supplement.lb554
Subject(s) - captopril , losartan , medicine , saline , chymase , triolein , mast cell , endocrinology , angiotensin ii , chemistry , receptor , immunology , blood pressure , biochemistry , lipase , enzyme
Fat embolism (FE) induced by IV injection of triolein (T) causes vasculitis, septal inflammation and fibrosis in rat lungs within 48 hrs (1). The damage is mitigated by two drugs acting on the renin‐angiotensin system (RAS): captopril and losartan (2). In the same organ, mast cell numbers are reduced in the lungs by losartan but not by captopril (3). This study examines whether captopril and losartan also modify the mast cell response in the liver. Methods Sprague‐Dawley rats (280–300g) were treated with 0.2ml iv (T) n=18 or saline n=7. One hour later 0.2ml of saline (n=6) ip, captopril (150 mg/kg n=6) or losartan (10mg/kg n=6) were given. Saline treated rats received ip, one hour later, the same does of saline. 48 hours later all the rats were necropsied after isoflurane anesthesia, lungs fixed in 10% formalin and H&E stained for morphology and CD117 for mast cells. Two pathologists unaware of the slides identity took at random 10 photographs of all the slides at 400× and separately counted the mast cells. Results As previously reported, 48 hours after triolein the lungs showed severe histopathological damage that was prevented by both RAS drugs and was associated with a high number of mast cells after captopril treatment but not by losartan (3). Similar results were observed in the liver where the mast cells after 48 hours of triolein treatment were statistically significantly increased (p=0.019) and even more when triolein treatment was associated with captopril (p=0.009). Mast cells numbers in the liver of losartan treated rats was however similar to that of controls and no statistically significant difference was observed. The overwhelming majority of mast cells were observed within the portal tract approximating 78%. The remaining were spread out within the hepatic parenchyma. Conclusion Mast cells may be involved in the pathological damage found after FE as suggested by their increase in number in the lungs and the liver after T and their reduction during protective treatment with losartan. However, the lack of effect of captopril on mast cell number at this acute period both in lungs and the liver may suggest that some other pathway may be involved in mast cell recruitment such as angiotensin 1–7. Support or Funding Information Supported by the Catherine T. Geldmacher Foundation, St. Louis MO. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .