Judy R. Kersten

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Recent evidence indicates that hyperglycemia is an important risk factor for the development of cardiovascular disease. We tested the hypothesis that myocardial infarct size is related to blood glucose concentration in the presence or absence of ischemic preconditioning (PC) stimuli in canine models of diabetes mellitus and acute hyperglycemia.(More)
published online Nov 2, 2009; J. Am. Coll. Cardiol. Kersten, Barbara Riegel, and John F. Robb Fleischmann, William K. Freeman, James B. Froehlich, Edward K. Kasper, Judy R. E. Joshua A. Beckman, Kenneth A. Brown, Hugh Calkins, Elliot L. Chaikof, Kirsten Society for Vascular Medicine, Society for Vascular Surgery, Lee A. Fleisher, Anesthesiologists, Society(More)
2007 WRITING COMMITTEE MEMBERS Lee A. Fleisher, MD, FACC, FAHA, Chair; Joshua A. Beckman, MD, FACC*; Kenneth A. Brown, MD, FACC, FAHA†; Hugh Calkins, MD, FACC, FAHA‡; Elliot L. Chaikof, MD§; Kirsten E. Fleischmann, MD, MPH, FACC; William K. Freeman, MD, FACC ; James B. Froehlich, MD, MPH, FACC; Edward K. Kasper, MD, FACC; Judy R. Kersten, MD, FACC¶; Barbara(More)
WRITING COMMITTEE MEMBERS Lee A. Fleisher, MD, FACC, FAHA, Chair; Joshua A. Beckman, MD, FACC¶; Kenneth A. Brown, MD, FACC, FAHA†; Hugh Calkins, MD, FACC, FAHA‡; Elliot L. Chaikof, MD#; Kirsten E. Fleischmann, MD, MPH, FACC; William K. Freeman, MD, FACC*; James B. Froehlich, MD, MPH, FACC; Edward K. Kasper, MD, FACC; Judy R. Kersten, MD, FACC§; Barbara(More)
A decrease in myofilament sensitivity to Ca2+ has been proposed as a mechanism for reversible contractile dysfunction after ischemia and reperfusion. The direct actions of intracoronary myofilament Ca2+ sensitizers on stunned myocardium have not been examined. Barbiturate-anesthetized dogs (n = 9) were instrumented for measurement of left ventricular (LV)(More)
UNLABELLED We tested the hypothesis that levosimendan, a new positive inotropic drug that activates adenosine triphosphate-regulated potassium (K(ATP)) channels in vitro, decreases myocardial infarct size in vivo. Myocardial infarct size was measured after a 60-min left anterior descending coronary artery occlusion and 3 h of reperfusion in dogs receiving(More)
BACKGROUND The authors tested the hypothesis that isoflurane directly preconditions myocardium against infarction via activation of K(ATP) channels and that the protection afforded by isoflurane is associated with an acute memory phase similar to that of ischemic preconditioning. METHODS Barbiturate-anesthetized dogs (n = 71) were instrumented for(More)
BACKGROUND Brief episodes of ischemia during early reperfusion after coronary occlusion reduce the extent of myocardial infarction. Phosphatidylinositol-3-kinase (PI3K) signaling has been implicated in this "postconditioning" phenomenon. The authors tested the hypothesis that isoflurane produces cardioprotection during early reperfusion after myocardial(More)
BACKGROUND The anesthetic noble gas, xenon, produces cardioprotection. We hypothesized that other noble gases without anesthetic properties [helium (He), neon (Ne), argon (Ar)] also produce cardioprotection, and further hypothesized that this beneficial effect is mediated by activation of prosurvival signaling kinases [including(More)
Ischemic preconditioning provides a powerful means to reduce myocardial infarct size in vivo and has been proposed to limit the extent of myocardial infarction in patients. In contrast, hyperglycemia correlates with increases in mortality after acute myocardial infarction. Thus we hypothesized that acute hyperglycemia alters the protection afforded by(More)