Abstract
It has been shown in many studies (for review see1) that occlusion of a left coronary descending artery in an initial phase produces ultrastructural symptoms of myocardial ischemia that finally pass the phase from reversible to irreversible injury, i.e. infarction. Duration of coronary artery occlusion, actual oxygen consumption of the left ventricle, and absence or presence of collateral perfusion have been shown2 to be factors modifying the speed of development of infarction, but after 24–48 hrs the final infarct size of 80% of the area at risk will, nevertheless, be present. Collateral blood vessels apparently do not influence very significantly final infarct size, but they greatly modify the process of infarction, as will be described in the following text. All data relate to ultrastructural observations made on cardiac tissue from dog hearts subjected to experimental myocardial infarction by occlusion of a coronary artery.
Keywords
- Coronary Artery Occlusion
- Neutrophil Granulocyte
- Collateral Blood Flow
- Experimental Myocardial Infarction
- Ischemic Zone
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References
Schaper, Jutta, Ultrastructural changes of the myocardium in regional ischemia and infarction, in: “Experimental Myocardial Ischemia and Infarction,” W. Schaper, ed., Marcel Dekker, New York, in press (1982).
W. Schaper, The Pathophysiology of Myocardial Infarction, Elsevier/North-Holland Biomedical Press, Amsterdam, New York, Oxford (1979).
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© 1984 Springer Science+Business Media New York
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Schaper, J. (1984). Fate of the Coronary Microvasculature in Infarcting Canine Myocardium: Role of Collateral Blood Flow. In: Chazov, E.I., Smirnov, V.N., Oganov, R.G. (eds) Cardiology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1824-9_43
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DOI: https://doi.org/10.1007/978-1-4757-1824-9_43
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