Nicotinamide mononucleotide preserves mitochondrial function and increases survival in hemorrhagic shock

We demonstrate that nicotinamide mononucleotide substantially mitigates inflammation, improves cellular metabolism, and promotes survival following hemorrhagic shock

Carrie A. Sims; Yuxia Guan; Sarmistha Mukherjee; Khushboo Singh; Paul Botolin; Antonio Davila; Joseph A. Baur


Scholarcy highlights

  • Hemorrhagic shock is a physiologic condition that occurs with rapid blood loss and is characterized by profound vasoconstriction, tissue hypoperfusion, and cellular hypoxia
  • Nicotinamide adenine dinucleotide is a ubiquitous molecule that plays a key role in cellular metabolism by accepting and donating electrons via interconversion with NADH
  • The dose of nicotinamide mononucleotide was proportional to body weight, and the volume of resuscitation was 4 times the volume of blood shed during hemorrhagic shock
  • During prolonged hypoperfusion there is a dramatic decline in nicotinamide adenine dinucleotide availability due to both a reduction in the size of the NAD pool and a shift toward the reduced form
  • Given the essential roles that NAD plays in glycolysis, oxidative phosphorylation, and pathways that promote cellular resilience, we investigated the possible benefit of using NMN to restore NAD levels as a treatment for hemorrhagic shock
  • NMN could positively affect many tissues in our model, we focused on the effect on bioenergetics in the kidney and liver, because these organs are at a high risk of failure following acute blood loss
  • In a separate set of experiments, animals pretreated with water only were subjected to decompensated hemorrhagic shock as previously described and resuscitated with 4 times the shed volume in LR plus nicotinamide mononucleotide over 60 minutes and followed for an additional 48 hours

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