Nitrite Anion Provides Potent Cytoprotective and Antiapoptotic Effects as Adjunctive Therapy to Reperfusion for Acute Myocardial Infarction
Open accessAbstract
Background— Accumulating evidence suggests that the ubiquitous anion nitrite (NO 2 − ) is a physiological signaling molecule, with roles in intravascular endocrine nitric oxide transport, hypoxic vasodilation, signaling, and cytoprotection. Thus, nitrite could enhance the efficacy of reperfusion therapy for acute myocardial infarction. The specific aims of this study were (1) to assess the efficacy of nitrite in reducing necrosis and apoptosis in canine myocardial infarction and (2) to determine the relative role of nitrite versus chemical intermediates, such as S -nitrosothiols. Methods and Results— We evaluated infarct size, microvascular perfusion, and left ventricular function by histopathology, microspheres, and magnetic resonance imaging in 27 canines subjected to 120 minutes of coronary artery occlusion. This was a blinded, prospective study comparing a saline control group (n=9) with intravenous nitrite during the last 60 minutes of ischemia (n=9) and during the last 5 minutes of ischemia (n=9). In saline-treated control animals, 70±10% of the area at risk was infarcted compared with 23±5% in animals treated with a 60-minute nitrite infusion. Remarkably, a nitrite infusion in the last 5 minutes of ischemia also limited the extent of infarction (36±8% of area at risk). Nitrite improved microvascular perfusion, reduced apoptosis, and improved contractile function. S -Nitrosothiol and iron-nitrosyl-protein adducts did not accumulate in the 5-minute nitrite infusion, suggesting that nitrite is the bioactive intravascular nitric oxide species accounting for cardioprotection. Conclusions— Nitrite has significant potential as adjunctive therapy to enhance the efficacy of reperfusion therapy for acute myocardial infarction.
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Nitrite administered before or during cardiac ischemia protects cardiac function and attenuates infarct size in small and large animal models.
“Nitrite administered before or during cardiac ischemia has been shown to protect cardiac function and attenuate infarct size in a number of small and large animal models (226, 374, 864).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [374]
The nitrate/nitrite content of fruits and vegetables could contribute to their cardiovascular health benefits in animals and humans.
“the nitrate/nitrite content of the fruits and vegetables could contribute to their cardiovascular health benefits in animals [29,33,78,79,80,81,82,83] and humans [31,84,85,86].”
From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [78]
Low concentrations of nitrite mediate cytoprotection in a variety of tissues in animal models including heart, liver, brain, kidney, hindlimb, and human forearm.
“The efficacy of low concentrations of nitrite in mediating cytoprotection has been demonstrated in a variety of tissues in animal models including heart [8, 9, 55, 118–122] liver [9, 120, 123], brain [124–126], kidney [127, 128], hindlimb [129], and human forearm [23].”
From Mechanisms of nitrite bioactivation (2014) · cites this paper as [119]
Pretreatment with sodium nitrite protects against ischemia/reperfusion injury in the heart in preclinical models.
“pretreatment with this compound, delivered as a salt in the form of sodium nitrite, protects against ischemia/reperfusion (I/R) injury in the heart in preclinical models (7, 19, 20, 40, 46, 60, 79, 189).”
From Inorganic nitrite supplementation for healthy arterial aging (2014) · cites this paper as [60]
Even after 5 minutes of reperfusion, nitrite therapy confers myocardial cytoprotection.
“Gonzalez et al demonstrated that even after 5 minutes of reperfusion nitrite therapy conferred myocardial cytoprotection [160].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [160]
Nitrite therapy has therapeutic potential in a myocardial ischemia-reperfusion model in dogs.
“cytoprotective effects were also examined using a myocardial ischemia-reperfusion model in dogs, further illustrating the therapeutic potential for this molecule [160].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [160]
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- Authors
- Gonzalez, F. M., Shiva, S., Vincent, P. S., Ringwood, L. A., Hsu, L.-Y., Hon, Y. Y., Aletras, A. H., Cannon, R. O., Gladwin, M. T., & Arai, A. E.
- Affiliations
- National Institutes of Health (US)
- ORCID
- Venue
- Circulation
- Published
- 2008-06-10
- Volume
- 117
- Issue
- 23
- Pages
- 2986-2994
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC2587279
- OpenAlex
- W1993541391
- Cited by
- 175
- References
- 47
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 4 · 2019: 6 · 2018: 5 · 2017: 9 · 2016: 8 · 2015: 15 · 2014: 14 · 2013: 17 · 2012: 11
- FWCI
- 15.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- National Institutes of Health (Z99 HL999999)
- National Heart, Lung, and Blood Institute (ZIAHL006136, Z01HL004607, ZIAHL005111, ZIAHL005112)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Keywords
- nitrite, acute myocardial infarction, reperfusion therapy, cardioprotection, apoptosis, infarct size, nitric oxide, S-nitrosothiols, microvascular blood flow, left ventricular function, coronary artery occlusion, canine model
- MeSH terms
- Animals, Anions, Cardiotonic Agents, Disease Models, Animal, Dogs, Hemoglobins, Magnetic Resonance Imaging, Myocardial Infarction, Necrosis, Nitric Oxide, Nitrites, Signal Transduction, Myocardial Reperfusion, Ventricular Function, Left, Apoptosis, Cytoprotection, S-Nitrosothiols, Myocytes, Cardiac
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