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1 e more compliant walls containing viable but stunned myocardium.
2 rylated phospholamban monomer was reduced in stunned myocardium.
3 protein troponin I has been correlated with stunned myocardium.
4 ponsiveness, recapitulating the phenotype of stunned myocardium.
5 rinol+MPG antioxidant cocktail in a model of stunned myocardium.
6 radation pattern similar to that observed in stunned myocardium.
7 ocardial infarction and five had evidence of stunned myocardium.
8 ared the results with the pathophysiology of stunned myocardium.
9 decreased myofilament Ca2+ responsiveness in stunned myocardium.
10 that Ca2+ channel activity is diminished in stunned myocardium.
11 rdium, which is distinct from hibernating or stunned myocardium.
12 TnI is partially and selectively degraded in stunned myocardium; (2) this degradation could be preven
16 version power Doppler techniques, identifies stunned myocardium, and accurately predicts recovery of
17 a central role in ischemic preconditioning, stunned myocardium, and in anesthetic-induced protection
20 he increase of end-systolic fiber lengths in stunned myocardium had no significant transmural gradien
21 that arising from viable (hibernating and/or stunned) myocardium has important implications for the m
23 ckers have been shown to enhance function of stunned myocardium in experimental studies, and in a few
25 te that the decreased Ca2+ responsiveness of stunned myocardium is due to intrinsic alterations of th
28 rates across the mitochondrial membranes of stunned myocardium, particularly through the reversible
29 ed SR gene expression and TnI degradation in stunned myocardium produced by 10-minute total left ante
30 show that the reduced Ca2+ responsiveness of stunned myocardium reflects alteration of the myofilamen
31 at the time course of functional recovery of stunned myocardium reflects the resynthesis of reversibl
33 epicardium, reflecting that this response in stunned myocardium was proportional to the severity of t
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