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Circulating nitrite contributes to cardioprotection by remote ischemic preconditioning.

Tienush Rassaf1, Matthias Totzeck, Ulrike B Hendgen-Cotta

  • 1From the Department of Medicine, Division of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty, University Hospital Duesseldorf, Duesseldorf, Germany (T.R., M.T., U.B.H.-C., M.K.); Department of Pharmacology and Chemical Biology, University of Pittsburgh, PA (S.S.); Institute for Pathophysiology, University of Essen, Essen, Germany (G.H.); and Cardiovascular Research Institute Duesseldorf, Duesseldorf, Germany (M.K.).

Circulation Research
|March 20, 2014
PubMed
Summary
This summary is machine-generated.

Remote ischemic preconditioning (rIPC) protects the heart by increasing circulating nitrite. This nitrite, generated in a remote limb, reduces heart damage after ischemia and reperfusion (I/R).

Keywords:
myocardialmyoglobinnitric oxide synthase type III

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Area of Science:

  • Cardiovascular Physiology
  • Ischemia-Reperfusion Injury
  • Nitric Oxide Signaling

Background:

  • Remote ischemic preconditioning (rIPC) protects the heart from injury.
  • The exact signaling pathways for rIPC's remote protective effects are not fully understood.

Purpose of the Study:

  • To investigate the role of circulating nitrite in cardioprotection mediated by rIPC.

Main Methods:

  • Mice underwent femoral artery ischemia/reperfusion (rIPC) followed by in vivo myocardial ischemia/reperfusion (I/R).
  • Genetic and pharmacological tools were used to manipulate nitric oxide/nitrite pathways.
  • Plasma transfer experiments from human volunteers subjected to rIPC were performed.

Main Results:

  • rIPC stimulated endothelial nitric oxide synthase, releasing nitrite humorally to the myocardium.
  • Cardiac myoglobin reduced nitrite to nitric oxide, protecting mitochondria and reducing infarct size.
  • Inhibiting nitrite generation or bioactivation abolished rIPC's cardioprotective effects.

Conclusions:

  • Circulating nitrite, produced at the remote ischemic site, is a key mediator of cardioprotection during myocardial I/R.
  • This finding clarifies a crucial mechanism of remote ischemic preconditioning.