The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Ischemic preconditioning alters real-time measure of O2 radicals in intact hearts with ischemia and reperfusion
Abstract
Reactive oxygen species (ROS) are believed to be involved in triggering cardiac ischemic preconditioning (IPC). Decreased formation of ROS on reperfusion after prolonged ischemia may in part underlie protection by IPC. In heart models, these contentions have been based either on the effect of ROS scavengers to abrogate IPC-induced preservation or on a measurement of oxidation products on reperfusion. Using spectrophotofluorometry at the left ventricular wall and the fluorescent probe dihydroethidium (DHE), we measured intracellular ROS superoxide (O[Formula: see text]·) continuously in isolated guinea pig heart and tested the effect of IPC and the O[Formula: see text]· scavenger manganese(III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP) on O[Formula: see text]· formation throughout the phases of preconditioning (PC), 30-min ischemia and 60-min reperfusion (I/R). IPC was evidenced by improved contractile function and reduced infarction; MnTBAP abrogated these effects. Brief PC pulses increased O[Formula: see text]· during the ischemic but not the reperfusion phase. O[Formula: see text]· increased by 35% within 1 min of ischemia, increased further to 95% after 20 min of ischemia, and decreased slowly on reperfusion. In the IPC group, O[Formula: see text]· was not elevated over 35% during index ischemia and was not increased at all on reperfusion; these effects were abrogated by MnTBAP. Our results directly demonstrate how intracellular ROS increase in intact hearts during IPC and I/R and clarify the role of ROS in triggering and mediating IPC.
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“A small class of “uncoupling” proteins, called UCPs 1–4, are believed to induce an inward proton “leak” in charged mitochondria (49, 55, 176, 300).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [176]
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Metadata
- Authors
- Kevin, L. G., Camara, A. K. S., Riess, M. L., Novalija, E., & Stowe, D. F.
- Affiliations
- Anesthesiology Research Laboratories, Departments ofAnesthesiology and
- Medical College of Wisconsin (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2003-02-01
- Volume
- 284
- Issue
- 2
- Pages
- H566-H574
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2079438155
- Cited by
- 272
- References
- 56
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 9 · 2018: 9 · 2017: 15 · 2016: 7 · 2015: 15 · 2014: 15 · 2013: 9 · 2012: 12
- FWCI
- 11.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL 58691, R01HL058691)
- National Institute of General Medical Sciences (GM-8204-06)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
- Keywords
- ischemic preconditioning, reactive oxygen species, superoxide, myocardial ischemia-reperfusion injury, MnTBAP, dihydroethidium, cardioprotection, myocardial infarction, guinea pig heart
- MeSH terms
- Animals, Computer Systems, Ethidium, Guinea Pigs, Myocardial Infarction, Myocardium, Spectrometry, Fluorescence, Myocardial Reperfusion Injury, Myocardial Ischemia, Reactive Oxygen Species, Ischemic Preconditioning, Myocardial, In Vitro Techniques
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