Cited by 484Cardiac Ischemia and ReperfusionOrgan Transplantation Techniques and OutcomesNitric Oxide and Endothelin Effects

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Oxygen Radicals Released During Ischemic Preconditioning Contribute to Cardioprotection in the Rabbit Myocardium

Baines, Christopher P., Goto, Mahiko, Downey, James M.·1997·Journal of Molecular and Cellular Cardiology

DOI 10.1006/jmcc.1996.0265

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Abstract

Previous studies have proposed that oxygen radicals may play a role in the triggering of ischemic preconditioning. However, studies evaluating the effects of radical scavengers have yielded conflicting results, possibly because of differences in the number of preconditioning episodes used. The present study tested whether N-2-mercaptopropionylglycine (MPG) could block protection of both single and multiple episodes of preconditioning in in situ and in vitro rabbit hearts. All hearts were subjected to 30 min of regional ischemia followed by reperfusion for 2 (in vitro) or 3 (in situ) h. Infarct size was measured by tetrazolium. Infarction in control in situ hearts was 37.5+/-3.5% of the risk zone. A single cycle of preconditioning (PC1), with 5 min ischemia/10 min reperfusion, reduced infarct size to 12.3+/-2.0% (P<0.05). Four cycles of preconditioning (PC4) were equally protective. MPG (1 mg/kg/min i.v.) alone had no effect on infarction but abolished protection afforded by PC1 (35.4+/-3.9%). However, MPG failed to block protection in the PC4 group. In isolated control hearts, infarct size was 31.1+/-1.8% and was reduced to 10.2+/-2.2% (P<0.05) by preconditioning. MPG (300 microM) aborted protection. Infusion of hypoxanthine or xanthine oxidase separately in lieu of preconditioning had no effect on infarct size, but induced protection when combined (14.1+/-2.2%; P<0.05). Polymyxin B, an inhibitor of protein kinase C (PKC), abolished this protection (53.1+/-4.1%). In conclusion, oxygen radicals contribute to ischemic preconditioning in the rabbit and appear to do so via activation of PKC. The fact that MPG could not block protection by PC4 suggests that oxygen radicals act in concert with other triggers of preconditioning such as adenosine and bradykinin.

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Background

Authors: Baines, C. P., Goto, M., & Downey, J. M.
Affiliations: University of South Alabama (US)
ORCID: Baines, Christopher P.
Downey, James M.
Venue: Journal of Molecular and Cellular Cardiology
Publisher: Elsevier BV
Published: 1997-01
Volume: 29
Issue: 1
Pages: 207-216
ISSN: 0022-2828 (ISSN-L)
DOI: 10.1006/jmcc.1996.0265
OpenAlex: W2122501550
Cited by: 484
References: 0
Citations by year: 2025: 1 · 2023: 1 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 8 · 2018: 8 · 2017: 11 · 2016: 12 · 2015: 12 · 2014: 16 · 2013: 21 · 2012: 18
FWCI: 13.61
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)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: ischemic preconditioning, oxygen free radicals, cardioprotection, protein kinase C, infarct size, myocardial ischemia-reperfusion injury, xanthine oxidase, hypoxanthine, adenosine, bradykinin, radical scavengers
MeSH terms: Analysis of Variance, Animals, Enzyme Activation, Female, Free Radicals, Hemodynamics, Male, Tiopronin, Myocardial Infarction, Protein Kinase C, Rabbits, Free Radical Scavengers, Reactive Oxygen Species, Ischemic Preconditioning, Myocardial, In Vitro Techniques

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Oxygen Radicals Released During Ischemic Preconditioning Contribute to Cardioprotection in the Rabbit Myocardium

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