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Cited by 171Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsOrgan Transplantation Techniques and Outcomes

Exogenous nitric oxide can trigger a preconditioned state through a free radical mechanism, but endogenous nitric oxide is not a trigger of classical ischemic preconditioning

Nakano, Atsushi, Liu, Guang S, Heusch, Gerd, Downey, James M, Cohen, Michael V·2000·Journal of Molecular and Cellular Cardiology
DOI 10.1006/jmcc.2000.1152
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Abstract

Nitric oxide (NO) has been reported to play an important role in the late phase of ischemic preconditioning (PC) in the rabbit heart. However, the role of NO in the early phase of ischemic PC ("classical PC") is controversial. Accordingly, the present study was designed to determine whether NO contributes to the cardioprotective effect of classical PC in rabbits. Isolated hearts experienced 30 min of regional ischemia followed by 120 min of reperfusion. Infarct size was measured with triphenyltetrazolium chloride. In control hearts infarction was 30.2+/-3.3% of the risk zone. PC with 5 min of global ischemia and 10 min of reperfusion reduced infarct size to 10.2+/-2.4% (P<0.05). Perfusion with 2 microm S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, in lieu of ischemia mimicked PC (4.4+/-1.9% infarction, P<0.01 v control). To determine whether this protection was dependent on either protein kinase C (PKC) as has previously been demonstrated for classical PC or free radicals known to be produced during exogenous NO administration, chelerythrine (5 microm), a PKC inhibitor, or N-(2-mercaptopropionyl)-glycine (300 microm), a free radical scavenger, was administered with or shortly after SNAP. Neither drug had any independent effect on infarct size, and each blocked SNAP's cardioprotection (31.0+/-5.1 and 25.7+/-5.2% infarction, resp.). N(omega)-nitro- L -arginine methyl ester (L -NAME, 100 microm), a NO synthase inhibitor, failed to block the cardioprotection from the above ischemic PC protocol (9.5+/-2.8% infarction, P<0.05 v control). L -NAME alone had no effect on infarct size (30.6+/-2.7%). These results suggest that the beneficial effect of exogenous NO production during SNAP pretreatment is mediated by a protein kinase C-dependent pathway via MPG-sensitive oxidants. However, we were unable to show any contribution of endogenous NO to classical PC's protection in isolated rabbit hearts.

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  • NOS ability to generate NO during ischemia is compromised because of the requirement for oxygen, BH4, and other co-factors that may be limiting during tissue ischemia.

    “Although NO is known to protect tissues from ischemic injury, the ability of nitric oxide synthases to generate NO during ischemia is compromised because of the requirement for oxygen, BH4, and other co-factors which may be limiting during tissue ischemia [29–31].”

    From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [29]

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Authors
Nakano, A., Liu, G. S., Heusch, G., Downey, J. M., & Cohen, M. V.
Affiliations
  • University of South Alabama (US)
  • Stiftung Universitätsmedizin Essen (DE)
Corresponding author
Cohen, Michael V
ORCID
Venue
Journal of Molecular and Cellular Cardiology
Publisher
Elsevier BV
Published
2000-07
Volume
32
Issue
7
Pages
1159-1167
ISSN
0022-2828 (ISSN-L)
DOI
10.1006/jmcc.2000.1152
OpenAlex
W2038367443
Semantic Scholar
2e56ce0aa902143915c04af510144ddd5622abf5
Cited by
171
References
51
Citations by year
2026: 1 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 4 · 2016: 3 · 2015: 4 · 2014: 2 · 2013: 10 · 2012: 6
FWCI
9.50
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Molecular and Cellular Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (HL20648, R01HL050688, HL50688, R01HL020648)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
Keywords
ischemic preconditioning, nitric oxide, free radicals, protein kinase C, cardioprotection, myocardial infarct size, ischemia-reperfusion injury, S-nitroso-N-acetylpenicillamine, NADPH oxidase, chelerythrine, N-(2-mercaptopropionyl)glycine, L-NAME, nitric oxide synthase
MeSH terms
Animals, Antioxidants, Enzyme Inhibitors, Female, Free Radicals, Glycine, Heart, Hemodynamics, Male, Myocardial Infarction, Myocardium, Nitric Oxide, Penicillamine, Protein Kinase C, Rabbits, Sulfhydryl Compounds, Ischemic Preconditioning, Myocardial, NG-Nitroarginine Methyl Ester, Nitric Oxide Donors

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