Humoral Mediators of Remote Ischemic Conditioning: Important Role of eNOS/NO/Nitrite

Acta Neurochir Suppl. 2016:121:45-8. doi: 10.1007/978-3-319-18497-5_8.

Abstract

Remote ischemic conditioning (RIC) is a powerful cardioprotectant and neuroprotectant. The mechanism of protection likely involves circulating, blood-borne mediators that transmit the signal from the periphery to the brain. The neuroprotective effect of RIC may be partially related to improvements in cerebral blood flow (CBF). Nitrite is a key circulating mediator of RIC and may be a mediator of increased CBF and also mediate cytoprotection through its effects on nitrosylation of mitochondrial proteins such as complex I. Measuring plasma nitrite may serve as an important blood biomarker, and measuring CBF by techniques such as MRI arterial spin labeling (ASL) may be an ideal surrogate imaging biomarker in clinical trials of RIC.

Keywords: Nitric oxide synthase 3 (NOS 3); Nitric oxide, endothelial nitric oxide synthase (eNOS); Nitrite; Remote ischemic conditioning; Remote ischemic postconditioning; Remote ischemic preconditioning; ischemic preconditioning; preconditioning.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Brain Ischemia / metabolism*
  • Cerebrovascular Circulation*
  • Chemokine CXCL12 / metabolism
  • Humans
  • Interleukin-10 / metabolism
  • Ischemic Preconditioning*
  • MicroRNAs / metabolism
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type III / metabolism*
  • Nitrites / metabolism*

Substances

  • Chemokine CXCL12
  • MIRN144 microRNA, rat
  • MicroRNAs
  • Nitrites
  • Interleukin-10
  • Nitric Oxide
  • Nitric Oxide Synthase Type III