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Oxygen Radicals Released During Ischemic Preconditioning Contribute to Cardioprotection in the Rabbit Myocardium
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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“Although constitutively expressed, the HIF-1α subunit has a very short half-life in normoxic conditions because of its rapid hydroxylation by prolyl-4 hydroxylases (PH1–3) (12, 36).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [12]
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“While oxidative stress caused by high levels of ROS damages cellular components and has been linked to a myriad of pathologies, ROS at a lower concentration serve as important cellular signaling molecules in the maintenance of physiological functions (55) and in cardioprotection afforded by ischemic preconditioning (7…”
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BackgroundInfluentialIschemic Preconditioning in Cardiac Surgery
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“MPG was administered according to a previous study in anesthetized rabbits.(2) The entire protocol is shown in Figure 1.”
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“So-called ischemic preconditioning could actually be hypothesized to involve XO-generated oxidants (52, 53) and result in enhanced cellular antioxidant defense (54).”
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Key Cellular Effectors in ROS-Mediated Cardiac Diseases
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Metadata
- Authors
- Baines, C. P., Goto, M., & Downey, J. M.
- Affiliations
- University of South Alabama (US)
- 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)
- 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
- 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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