The renin inhibitor aliskiren protects rat lungs from the histopathological effects of fat embolism.

Background: Fat embolism (FE) and the consequent fat embolism syndrome (FES) occurring after trauma or surgery can lead to serious pulmonary injury, including ARDS and death. Current treatment of FES is limited to supportive therapy. We have shown in a rat model that the renin angiotensin system (RAS) plays a significant role in the pathophysiology of FE since drugs interfering with the RAS, captopril and losartan, reduce the histopathologic pulmonary damage. The purpose of the current study was to determine if inhibition of renin by aliskiren, an FDA-approved drug for treating hypertension, would produce effective protection in the same model. Methods: The FE model used intravenous injection of the neutral fat triolein in unanesthetized rats. Intraperitoneal injections of saline or aliskiren at either 50 mg/kg or 100 mg/kg were performed one hour after FE induction via triolein. Rats were euthanized at 48 hours and various histological stains were used to examine the lungs. Results: (1) Fibrosis: Rats treated with triolein showed significant fibrotic changes with increased collagen and myofibroblast activation (p

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