Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver.

@article{Duranski2005CytoprotectiveEO,
  title={Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver.},
  author={Mark R. Duranski and James J. M. Greer and A. Dejam and S. Jaganmohan and N. Hogg and W. Langston and R. Patel and S. yet and Xunde Wang and C. Kevil and M. Gladwin and D. Lefer},
  journal={The Journal of clinical investigation},
  year={2005},
  volume={115 5},
  pages={
          1232-40
        }
}
Nitrite represents a circulating and tissue storage form of NO whose bioactivation is mediated by the enzymatic action of xanthine oxidoreductase, nonenzymatic disproportionation, and reduction by deoxyhemoglobin, myoglobin, and tissue heme proteins. Because the rate of NO generation from nitrite is linearly dependent on reductions in oxygen and pH levels, we hypothesized that nitrite would be reduced to NO in ischemic tissue and exert NO-dependent protective effects. Solutions of sodium… Expand
Role of the anion nitrite in ischemia-reperfusion cytoprotection and therapeutics.
TLDR
The evidence of nitrite-mediated cytoprotection against IR injury in multiple animal models opens the door to potential therapeutic opportunities in human disease. Expand
Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer
TLDR
It is reported that both acute and delayed exposure to physiological concentrations of nitrite, given both systemically or orally, potently limits cardiac and hepatic reperfusion injury and may represent an effector of the cell-survival program of ischemic preconditioning and the Mediterranean diet. Expand
Nitrite Anion Provides Potent Cytoprotective and Antiapoptotic Effects as Adjunctive Therapy to Reperfusion for Acute Myocardial Infarction
TLDR
Nitrite has significant potential as adjunctive therapy to enhance the efficacy of reperfusion therapy for acute myocardial infarction and is the bioactive intravascular nitric oxide species accounting for cardioprotection. Expand
Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase–dependent manner
TLDR
It is shown that nitrite can protect against toxicity in shock via sGC-dependent signaling, which may include hypoxic vasodilation necessary to maintain microcirculation and organ function, and cardioprotection. Expand
The cytoprotective effect of nitrite is based on the formation of dinitrosyl iron complexes.
TLDR
Evidence is provided that upon hypoxia, mitochondria reduce nitrite to nitric oxide (NO) in amounts sufficient to inactivate redox-active iron ions by formation of inactive dinitrosyl iron complexes (DNIC), suggesting that the formation of DNIC is a key mechanism of nitrite-mediated cytoprotection. Expand
Nitrite is a vascular store of NO which mediates hypoxic signaling and protects against ischemia/reperfusion injury
Abstract The circulating anion nitrite, once thought to be a physiologically inert byproduct of nitric oxide (NO) oxidation, has been proposed to be a vascular storage form of bioactive NO. NitriteExpand
Nitrite-derived nitric oxide protects the rat kidney against ischemia/reperfusion injury in vivo: role for xanthine oxidoreductase.
TLDR
It is demonstrated that topically administered sodium nitrite protects the rat kidney against I/R injury and dysfunction in vivo via the generation, in part, of xanthine oxidoreductase-catalyzed NO production. Expand
Dietary nitrite supplementation protects against myocardial ischemia-reperfusion injury
TLDR
The significant influence of dietary nitrite and nitrate intake on the maintenance of steady-state tissue nitrite/nitroso levels is demonstrated and the consequences of nitrite deficiency on the pathophysiology of MI/R injury are illustrated. Expand
Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I
TLDR
The results identify rapid complex I reactivation as a central pathological feature of ischemia-reperfusion injury and show that preventing this reactivation by modification of a cysteine switch is a robust cardioprotective mechanism and hence a rational therapeutic strategy. Expand
Formation and role of plasma S-nitrosothiols in liver ischemia-reperfusion injury.
TLDR
Investigating the changes in plasma RSNOs following liver I/R injury suggests that significant upregulation of nitric oxide synthesis during the late phase of reperfusion is associated with impairment in microcirculation and mitochondrial dysfunction. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 74 REFERENCES
Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage.
Nitric oxide (NO.) is thought to protect against the damaging effects of myocardial ischemia-reperfusion injury, whereas xanthine oxidoreductase (XOR) normally causes damage through the generation ofExpand
Nitrosyl-Heme Complexes Are Formed in the Ischemic Heart
In addition to the generation from specific nitric-oxide (NO) synthases, NO formation from nitrite occurs in ischemic tissues, such as the heart. Although NO binding to heme-centers is the basis forExpand
Attenuation of myocardial ischemia/reperfusion injury by superinduction of inducible nitric oxide synthase.
TLDR
No protects against I/R injury by preventing the hyperdynamic response of isolated perfused hearts during early reperfusion, accompanied by a superinduction of iNOS, possibly due to an adaptive mechanism. Expand
Regulation of postischemic liver injury following different durations of ischemia.
TLDR
It is concluded that the sources for O(2)(-) formation and the relative importance of TNF-alpha in the pathophysiology of I/R-induced hepatocellular injury differ depending on the duration of ischemia. Expand
Mitochondria as Targets for Nitric Oxide-Induced Protection During Simulated Ischemia and Reoxygenation in Isolated Neonatal Cardiomyocytes
TLDR
Pretreatment with an NO donor induces a modest, sustained mitochondrial depolarization and protects cardiomyocytes from sI/R injury, possibly reduces cytosolic Ca2+ overload, providing a likely mechanism for NO-induced protection. Expand
Antineutrophil and Myocardial Protecting Actions of a Novel Nitric Oxide Donor After Acute Myocardial Ischemia and Reperfusion in Dogs
TLDR
SPM-5185 reduces myocardial necrosis and neutrophil accumulation in an acute model of canineMyocardial ischemia and reperfusion and may be partially related to the inhibitory actions of this novel NO donor on neutrophils adherence to the coronary endothelium. Expand
Nitrite reduction to nitric oxide by deoxyhemoglobin vasodilates the human circulation
TLDR
It is suggested that nitrite represents a major bioavailable pool of NO, and a new physiological function for hemoglobin as a nitrite reductase is described, potentially contributing to hypoxic vasodilation. Expand
Inhibition of nitric oxide synthesis protects the isolated working rabbit heart from ischaemia-reperfusion injury.
TLDR
The recovery of mechanical function of hearts subjected to ischaemia-reperfusion injury can be improved by modulation of myocardial NO synthesis, and inhibition of NO synthesis (with L-NAME or L-NMMA) may offer prolonged protection whereas its stimulation provides only brief protection. Expand
Inhibition of nitric oxide synthesis reduces infarct size by an adenosine-dependent mechanism.
TLDR
In this model, infarct size limitation after inhibition of NO synthesis shares a common mechanism with that of ischemic preconditioning and is dependent on the release of adenosine, however, in this model the protection of the heart against ischemia-reperfusion injury by adenosines appears to be concentration dependent. Expand
Enhanced post-ischemic liver injury in iNOS-deficient mice: a cautionary note.
TLDR
It is found that partial hepatic ischemia involving 70% of the liver resulted in a time-dependent increase in serum alanine aminotransferase levels at 1-6 h following reperfusion, and iNOS deficiency produces unanticipated genetic alterations that renders these mice more sensitive to liver I/R-induced injury. Expand
...
1
2
3
4
5
...