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The “No-Reflow” Phenomenon after Temporary Coronary Occlusion in the Dog
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The role of microvascular damage in the genesis of the "no-reflow" phenomenon was investigated in the left ventricular myocardium of dogs subjected to temporary occlusions of a major coronary artery for 40 and 90 min. Intravenous carbon black or thioflavin S (a fluorescent vital stain for endothelium) were used to demonstrate the distribution of coronary arterial flow in control and damaged myocardium. These tracers were injected simultaneously with release of the coronary occlusion or after 5 or 20 min of reflow of coronary arterial blood. After 40 min of ischemia plus arterial reperfusion, usually the tracers were evenly distributed throughout the damaged tissue at each time of reperfusion. On the other hand, when reflow was allowed after 90 min of ischemia, portions of the inner half of damaged myocardium were not penetrated by the tracers. Electron microscopic study of this poorly perfused tissue revealed severe capillary damage; endothelial cells with large intraluminal protrusions and decreased pinocytic vesicles were common. Also, occasional intraluminal fibrin thrombi were noted, as well as extravascular fibrin deposits and erythrocytes. Myocardial cells were swollen in both poorly perfused and well-perfused irreversibly injured tissue. Contraction bands and mitochondrial Ca(2+) accumulation were prominent features of irreversible injury with reflow at 40 min but were not noted after 90 min of ischemia in areas with poor perfusion. These results suggest that 40 min of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or perfusion defects, but that 90 min of ischemic injury was associated with the "no-reflow" phenomenon, i.e., failure to achieve uniform reperfusion. This failure of reflow was associated with extensive capillary damage and myocardial cell swelling. Death of severely ischemic myocardial cells in this model occurs before the onset of capillary damage and the no-reflow phenomenon.
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“The apoptosis induces endothelial swelling, microvascular spasms, and capillary obstruction, which slows or even stops microcirculation blood flow following reperfusion [179].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [179]
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“I/R injury is primarily induced by endothelial cell apoptosis in microcirculation.”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [179]
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Metadata
- Authors
- Kloner, R. A., Ganote, C. E., & Jennings, R. B.
- Affiliations
- Northwestern University (US)
- ORCID
- Kloner, Robert A.
- Venue
- Journal of Clinical Investigation
- Published
- 1974-12-01
- Volume
- 54
- Issue
- 6
- Pages
- 1496-1508
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC301706
- OpenAlex
- W2140233303
- Cited by
- 1,842
- References
- 25
- Citations by year
- 2026: 21 · 2025: 25 · 2024: 28 · 2023: 30 · 2022: 37 · 2021: 37 · 2020: 30 · 2019: 44 · 2018: 36 · 2017: 35 · 2016: 53 · 2015: 53 · 2014: 43 · 2013: 46 · 2012: 55
- FWCI
- 12.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart and Lung Institute
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- no-reflow phenomenon, myocardial ischemia, myocardial reperfusion, capillary damage, irreversible myocardial injury, coronary artery occlusion, thioflavin S, fibrin thrombi, mitochondrial calcium accumulation, contraction bands, ischemic tolerance
- MeSH terms
- Animals, Capillaries, Carbon, Coronary Circulation, Coronary Disease, Coronary Vessels, Dogs, Erythrocytes, Female, Fluorescence, Fluorescent Dyes, Ischemia, Male, Microcirculation, Microscopy, Electron, Mitochondria, Muscle, Myocardium, Papillary Muscles, Staining and Labeling, Thiazoles, Time Factors
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