Key result
In a canine model, 6 hours of severe myocardial ischemia significantly reduced epicardial (Na+ + K+)-ATPase catalytic activity to 61.3% of nonischemic levels, impairing cardiac glycoside binding.
Why the study?
Does ischemia and reperfusion alter myocardial (Na+ + K+)-ATPase activity and cardiac glycoside binding in a canine model?
Population
34 dogs with anterior wall infarction produced by snaring of confluent branches of the left coronary system
Comparison
Coronary occlusion for 1, 2, or 6 hours followed… vs Nonischemic myocardium
Design
Preclinical
Follow-up
Up to 6 hours of occlusion followed by 45 minutes of…
Authors
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Prolonged ischemia may impair cardiac glycoside binding; leaves open human ATPase recovery after reperfusion.
Does ischemia and reperfusion alter myocardial (Na+ + K+)-ATPase activity and cardiac glycoside binding in a canine model?
Absolute Event Rate: 61.3% vs 100%
p-value: p=<0.001
Severe ischemia (≥2 hours) progressively diminishes myocardial (Na+ + K+)-ATPase catalytic activity and cardiac glycoside binding, which is not restored by short-term reperfusion.
Beller et al. (1976) studied Acute myocardial ischemia (n=34). Coronary occlusion (ischemia) and reperfusion vs. Nonischemic myocardium was evaluated on (Na+ + K+)-ATPase activity in epicardial layers after 6 hours of occlusion (as % of nonischemic activity) (p=<0.001). In a canine model, 6 hours of severe myocardial ischemia significantly reduced epicardial (Na+ + K+)-ATPase catalytic activity to 61.3% of nonischemic levels, impairing cardiac glycoside binding.
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