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Ann Surg. 2019 Jun 7. doi: 10.1097/SLA.0000000000003407. [Epub ahead of print]

Resolvin D1 Attenuates the Organ Injury Associated With Experimental Hemorrhagic Shock.

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Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine & Dentistry, London, UK.
Department of Pharmacology, Universidade Federal de Santa Catarina, Florianópolis, Brazil.
Department of Drug Science and Technology, University of Turin, Turin, Italy.
Department of Public Health and Pediatric Sciences, University of Turin, Italy.
Lipid Mediator Unit, Queen Mary University of London, William Harvey Research Institute, Barts and The London School of Medicine & Dentistry, London, UK.
Queen Mary University of London, Blizard Institute of Cell and Molecular Sciences, Barts and the London School of Medicine, London, UK.
Queen Mary University of London, Centre for Inflammation and Therapeutic Innovation, London, UK.



To evaluate the potential changes in the plasma levels of resolvin D1 (RvD1) in patients with trauma and hemorrhage. Having found that trauma results in a profound reduction in plasma RvD1 in patients, we have then investigated the effects of RvD1 on the organ injury and dysfunction associated with hemorrhagic shock (HS) in the rat.


HS is a common cause of death in trauma due to excessive systemic inflammation and multiple organ failure. RvD1 is a member of the resolvin family of pro-resolution mediators.


Blood samples were drawn from critically injured patients (n = 27, ACITII-prospective observational cohort study) within 2 hours of injury for targeted liquid chromatography tandem mass spectrometry. HS rats (removal of blood to reduce arterial pressure to 30 ± 2 mm Hg, 90 minutes, followed by resuscitation) were treated with RvD1 (0.3 or 1 μg/kg intravenous (i.v.)) or vehicle (n = 7). Parameters of organ injury and dysfunction were determined.


Plasma levels of RvD1 (mg/dL) were reduced in patients with trauma+HS (0.17 ± 0.08) when compared with healthy volunteers (0.76 ± 0.25) and trauma patients (0.62 ± 0.20). In rats with HS, RvD1 attenuated the kidney dysfunction, liver injury, and tissue ischemia. RvD1 also reduced activation of the nuclear factor (NF)-κB pathway and reduced the expression of pro-inflammatory proteins such as inducible nitric oxide synthase, tumor necrosis factor-α, interleukin-1β, and interleukin-6.


Plasma RvD1 is reduced in patients with trauma-HS. In rats with HS, administration of synthetic RvD1 on resuscitation attenuated the multiple organ failure associated with HS by a mechanism that involves inhibition of the activation of NF-κB.

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