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Critical Care |

Cardiac Damage in a Model of Pulmonary Fat Embolism FREE TO VIEW

Darwish Naji; Shehabaldin Alqalyoobi; Betty Herndon; Agostino Molteni, PhD; Gary Salzman
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Internal Medicine, University of Missouri-Kansas City, Overland Park, KS


Chest. 2014;146(4_MeetingAbstracts):207A. doi:10.1378/chest.1995023
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Abstract

SESSION TITLE: ARDS/Lung Injury Posters

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PM

PURPOSE: In humans fat embolism (FE: from marrow lipids reaching the lung secondary to long bone fracture) is seen early post injury as respiratory insufficiency which clears without intervention. It is commonly believed that there are no long term pulmonary sequelae after FE—although human studies have shown decreased PFTs in groups with healed long bone fractures compared to controls. This study continues our early work which showed rapid dilation of right ventricle after FE, which resolved in < 2 weeks.

METHODS: In the present study (28 male SD rats, approved by the University animal committee) 14 received IV triolein (FE model) or IV saline at 0 time. At 6 weeks losartan was given to half of each group as i.p. loading dose then in drinking water to week 10. At week 10, necropsy was performed, tissue was fixed in formalin. Histology / pathology was described from H&E - stained sections. 4-5 photos at 400x were made of each heart. Patency of the right ventricle was measured. Pathology of the heart was quantified at 400x by a pathologist unaware of slide identity.

RESULTS: Myocardium of triolein treated rats showed venous congestion (p<0.001 vs control), with increased number of inflammatory cells among the fibers. Coagulation necrosis with pyknotic nuclei and arteriolar vasculitis were more severe in triolein groups than with controls, p<0.001 and p<0.004. Losartan-treated rats receiving saline did not differ morphologically from controls. Losartan treated hearts did not show triolein-induced damage. Right ventricle-heart ratio showed a trend of dilation in triolein-treated animals which was not evident in losartan-treated animals

CONCLUSIONS: In the fat embolism model, in addition to the persisting lung pathology, the heart shows damage which was decreased by losartan.

CLINICAL IMPLICATIONS: Pulmonary fat embolism is complicated by myocardial damage in this model. As in the lung, losartan protects the heart from the triolein-induced damage.

DISCLOSURE: The following authors have nothing to disclose: Darwish Naji, Shehabaldin Alqalyoobi, Betty Herndon, Agostino Molteni, Gary Salzman

No Product/Research Disclosure Information


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