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Aliskiren Does Not Protect the Heart from the Acute Histopathological Effects of Fat Embolism when it Protects the Lungs

Fat embolism (FE) can lead to both acute and chronic lung injury. In an animal model of FE induced by Triolein, the histopathological damage was not limited to the lungs but also involved the heart and kidneys. We have previously demonstrated that losartan, an angiotensin receptor blocker, prevented the damage induced by FE in both the lungs and the heart at 10 weeks. We also identified significant pulmonary damage as early as 48 hours and it was prevented by the direct renin inhibitor, Aliskiren suggesting the role of Renin‐Angiotensin System (RAS) in the pathogenesis of fibrosis. In the current study we examined the acute effects of FE (48 hours) on the heart, the influence of Aliskiren on this organ and compared it to the effects on the lungs.