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Chapter 38: Molecular and Cellular Mechanisms of Myocardial Ischemia/Reperfusion Injury

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Which of the following is not a determinant of infarct size?

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A. Time to reperfusion

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B. The presence of collaterals

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C. Blood pressure

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D. Temperature

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E. Ischemia/reperfusion injury

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The answer is C. (Hurst’s The Heart, 14th Edition, Chap. 38) Shorter time to reperfusion and an increased number of collaterals are associated with smaller infarct sizes (options A and B). Lower temperatures and larger ischemia/reperfusion injury are associated with larger infarct sizes (options D and E). Blood pressure by itself is not directly associated with infarct size (option C).

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Which of the following does not contribute to myocyte necrosis after reperfusion?

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A. Sarcolemma disruption and calcium overload

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B. ATP depletion and reversal of the Na+/Ca2+ exchanger, resulting in increased intracellular calcium

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C. The no-reflow phenomenon

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D. Tissue edema

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E. Autophagy

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The answer is E. (Hurst’s The Heart, 14th Edition, Chap. 38) Calcium overload that results from disruption of the sarcolemma and reversal of the Na+/Ca2+ exchanger contribute to reperfusion injury (options A and B).1 Impairment of the microcirculation via the no-reflow phenomenon or by compression through tissue edema can exacerbate reperfusion injury (options C and D).2,3 Autophagy is not known to contribute to reperfusion injury (option E).

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Which of the following is true about intracellular Ca2+ during ischemia-reperfusion injury?

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A. The Na+/Ca2+ exchanger extrudes Ca2+ from the cytoplasm

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B. Calpains are activated by increases in Ca2+

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C. The RyR2 does not contribute to increased intracellular Ca2+

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D. Sarcolemma membranes remain intact

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E. Calpains are only active at low pH

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The answer is B. (Hurst’s The Heart, 14th Edition, Chap. 38) Altered Ca2+ handling is one of the most prominent and relevant aspects of cardiomyocyte reperfusion. Reperfusion causes further Ca2+ influx through the Na+/Ca2+ exchanger in response to Na+ overload (option A). An important consequence of increased Ca2+ is activation of the Ca2+-dependent proteases calpains. Calpains translocate to the sarcolemma during ischemia in response to Ca2+ overload but are activated ...

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