Novel Mechanisms Mediating Stunned Myocardium

[1]  C. Depré.  Gene Profiling in the Heart by Subtractive Hybridization , 2004 .

[2]  S. Vatner,et al.  A Novel Mechanism for Myocardial Stunning Involving Impaired Ca2+ Handling , 2001, Circulation research.

[3]  J. Whisstock,et al.  The Serpins Are an Expanding Superfamily of Structurally Similar but Functionally Diverse Proteins , 2001, The Journal of Biological Chemistry.

[4]  S. Vatner,et al.  Gene program for cardiac cell survival induced by transient ischemia in conscious pigs , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[5]  J. Canty,et al.  Preload Induces Troponin I Degradation Independently of Myocardial Ischemia , 2001, Circulation.

[6]  Wei Li,et al.  Effects of Early Angiotensin-Converting Enzyme Inhibition on Cardiac Gene Expression After Acute Myocardial Infarction , 2001, Circulation.

[7]  D. Atar,et al.  Cardiac Troponin I Is Modified in the Myocardium of Bypass Patients , 2001, Circulation.

[8]  B. Bluestein,et al.  Extensive troponin I and T modification detected in serum from patients with acute myocardial infarction. , 2000, Circulation.

[9]  F. Müller,et al.  Biochemical mechanism(s) of stunning in conscious dogs. , 2000, American journal of physiology. Heart and circulatory physiology.

[10]  S. Vatner,et al.  Nitric oxide, an important regulator of perfusion-contraction matching in conscious pigs. , 2000, American journal of physiology. Heart and circulatory physiology.

[11]  L. Stanton,et al.  Altered patterns of gene expression in response to myocardial infarction. , 2000, Circulation research.

[12]  K. Hillan,et al.  Application of cDNA microarrays in determining molecular phenotype in cardiac growth, development, and response to injury. , 2000, Circulation.

[13]  F. Klocke,et al.  Myofibrillar disruption in hypocontractile myocardium showing perfusion-contraction matches and mismatches. , 2000, American journal of physiology. Heart and circulatory physiology.

[14]  D. Kass,et al.  Transgenic mouse model of stunned myocardium. , 2000, Science.

[15]  R. Bolli,et al.  Nitric oxide donors attenuate myocardial stunning in conscious rabbits. , 1999, The American journal of physiology.

[16]  J. Canty,et al.  Absence of troponin I degradation or altered sarcoplasmic reticulum uptake protein expression after reversible ischemia in swine. , 1999, Circulation research.

[17]  D. Bers,et al.  Ca2+ handling and sarcoplasmic reticulum Ca2+ content in isolated failing and nonfailing human myocardium. , 1999, Circulation research.

[18]  J. Canty,et al.  Differential 18F-2-deoxyglucose uptake in viable dysfunctional myocardium with normal resting perfusion: evidence for chronic stunning in pigs. , 1999, Circulation.

[19]  J. Seidman,et al.  Altered cardiac excitation-contraction coupling in mutant mice with familial hypertrophic cardiomyopathy. , 1999, The Journal of clinical investigation.

[20]  S. Vatner,et al.  An adenosine agonist and preconditioning shift the distribution of myocardial blood flow in conscious pigs. , 1999, American journal of physiology. Heart and circulatory physiology.

[21]  D. K. Arrell,et al.  Troponin I degradation and covalent complex formation accompanies myocardial ischemia/reperfusion injury. , 1999, Circulation research.

[22]  A. Clerk,et al.  Cellular mechanisms of cardiac hypertrophy , 1998, Journal of Molecular Medicine.

[23]  S. Vatner,et al.  Hibernating myocardium. , 1998, The New England journal of medicine.

[24]  S. Vatner,et al.  Ineffective perfusion-contraction matching in conscious, chronically instrumented pigs with an extended period of coronary stenosis. , 1998, Circulation research.

[25]  E. Braunwald,et al.  Medical and cellular implications of stunning, hibernation, and preconditioning: an NHLBI workshop. , 1998, Circulation.

[26]  F. Müller,et al.  Expression of calcium regulatory proteins in short-term hibernation and stunning in the in situ porcine heart. , 1998, Cardiovascular research.

[27]  R. Hodges,et al.  Breakdown and release of myofilament proteins during ischemia and ischemia/reperfusion in rat hearts: identification of degradation products and effects on the pCa-force relation. , 1998, Circulation research.

[28]  J Knuuti,et al.  Pathophysiological mechanisms of chronic reversible left ventricular dysfunction due to coronary artery disease (hibernating myocardium). , 1997, Circulation.

[29]  Tsonwin Hai,et al.  Tissue-specific Pattern of Stress Kinase Activation in Ischemic/Reperfused Heart and Kidney* , 1997, The Journal of Biological Chemistry.

[30]  S. Vatner,et al.  Delayed enhanced nitric oxide-mediated coronary vasodilation following brief ischemia and prolonged reperfusion in conscious dogs. , 1997, Circulation research.

[31]  S. Vatner,et al.  Beta-adrenergic receptor signalling in stunned myocardium of conscious pigs. , 1997, Journal of molecular and cellular cardiology.

[32]  J. Canty,et al.  18F-2-deoxyglucose deposition and regional flow in pigs with chronically dysfunctional myocardium. Evidence for transmural variations in chronic hibernating myocardium. , 1997, Circulation.

[33]  D. Atar,et al.  Role of troponin I proteolysis in the pathogenesis of stunned myocardium. , 1997, Circulation research.

[34]  E. Kranias,et al.  Phospholamban deficiency alters inactivation kinetics of L-type Ca2+ channels in mouse ventricular myocytes. , 1997, The American journal of physiology.

[35]  S. Vatner,et al.  Inotropic reserve and histological appearance of hibernating myocardium in conscious pigs with ameroid-induced coronary stenosis , 1996, Basic Research in Cardiology.

[36]  D. Waters,et al.  Functional and structural alterations with 24-hour myocardial hibernation and recovery after reperfusion. A pig model of myocardial hibernation. , 1996, Circulation.

[37]  Yongge Liu,et al.  Intrinsic myofilament alterations underlying the decreased contractility of stunned myocardium. A consequence of Ca2+-dependent proteolysis? , 1996, Circulation research.

[38]  R. Bolli,et al.  Evidence for an essential role of reactive oxygen species in the genesis of late preconditioning against myocardial stunning in conscious pigs. , 1996, The Journal of clinical investigation.

[39]  R. Bolli,et al.  Recurrent ischemia in the canine heart causes recurrent bursts of free radical production that have a cumulative effect on contractile function. A pathophysiological basis for chronic myocardial "stunning". , 1995, Journal of Clinical Investigation.

[40]  E. Marbán,et al.  Stunned myocardium: a disease of the myofilaments , 1995, Basic Research in Cardiology.

[41]  D. Atar,et al.  Relationship between intracellular calcium and contractile force in stunned myocardium. Direct evidence for decreased myofilament Ca2+ responsiveness and altered diastolic function in intact ventricular muscle. , 1995, Circulation research.

[42]  S. Vatner,et al.  Mechanism of impaired myocardial function during progressive coronary stenosis in conscious pigs. Hibernation versus stunning? , 1995, Circulation research.

[43]  R. Kloner,et al.  Clinical evidence for stunned myocardium after coronary artery bypass surgery. , 1995, Journal of cardiac surgery.

[44]  M. Arras,et al.  Changes in gene expression following short coronary occlusions studied in porcine hearts with run-on assays. , 1994, Cardiovascular research.

[45]  E. Marbán,et al.  Myofilament Ca2+ sensitivity in intact versus skinned rat ventricular muscle. , 1994, Circulation research.

[46]  S. Vatner,et al.  Inhibition of Endothelium‐Derived Relaxing Factor Enhances Myocardial Stunning in Conscious Dogs , 1993, Circulation.

[47]  W. Schaper,et al.  Enhanced gene expression of calcium regulatory proteins in stunned porcine myocardium. , 1993, Cardiovascular research.

[48]  J. Thornby,et al.  Direct evidence that the hydroxyl radical plays a pathogenetic role in myocardial "stunning" in the conscious dog and demonstration that stunning can be markedly attenuated without subsequent adverse effects. , 1993, Circulation research.

[49]  R. Bolli,et al.  Use of aromatic hydroxylation of phenylalanine to measure production of hydroxyl radicals after myocardial ischemia in vivo. Direct evidence for a pathogenetic role of the hydroxyl radical in myocardial stunning. , 1993, Circulation research.

[50]  G. Heusch,et al.  Development of Short‐term Myocardial Hibernation Its Limitation by the Severity of Ischemia and Inotropic Stimulation , 1993, Circulation.

[51]  R. Currie,et al.  Heat‐Shock Response and Limitation of Tissue Necrosis During Occlusion/Reperfusion in Rabbit Hearts , 1993, Circulation.

[52]  W. Schaper,et al.  Proto-oncogene expression in porcine myocardium subjected to ischemia and reperfusion. , 1992, Circulation research.

[53]  W. Grossman,et al.  Decreased myofilament responsiveness in myocardial stunning follows transient calcium overload during ischemia and reperfusion. , 1992, Circulation research.

[54]  G. Heusch,et al.  Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation. , 1992, Circulation research.

[55]  J. Parratt,et al.  Antiarrhythmic effects of preconditioning in anaesthetised dogs and rats. , 1992, Cardiovascular research.

[56]  A. Arai,et al.  Active downregulation of myocardial energy requirements during prolonged moderate ischemia in swine. , 1991, Circulation research.

[57]  J. Thornby,et al.  Postischemic myocardial "stunning". Identification of major differences between the open-chest and the conscious dog and evaluation of the oxygen radical hypothesis in the conscious dog. , 1991, Circulation research.

[58]  V. P. Chacko,et al.  Glycolytic inhibition and calcium overload as consequences of exogenously generated free radicals in rabbit hearts. , 1991, The Journal of clinical investigation.

[59]  John W. Allen,et al.  Stunned left ventricular myocardium after exercise treadmill testing in coronary artery disease. , 1991, The American journal of cardiology.

[60]  S. Chierchia,et al.  Symptom-limited exercise testing causes sustained diastolic dysfunction in patients with coronary disease and low effort tolerance. , 1991, Journal of the American College of Cardiology.

[61]  Donald M. Bers,et al.  Excitation-Contraction Coupling and Cardiac Contractile Force , 1991, Developments in Cardiovascular Medicine.

[62]  E. Marbán,et al.  23Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion. , 1990, The American journal of physiology.

[63]  A. Arai,et al.  Regeneration of myocardial phosphocreatine in pigs despite continued moderate ischemia. , 1990, Circulation research.

[64]  J. Parratt,et al.  Protective effects of preconditioning of the ischaemic myocardium involve cyclo-oxygenase products. , 1990, Cardiovascular research.

[65]  A. Buda,et al.  Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction. , 1990, The American journal of cardiology.

[66]  R. Bolli.  Mechanism of Myocardial “Stunning” , 1990, Circulation.

[67]  V. P. Chacko,et al.  Quantification of [Ca2']i in Perfused Hearts Critical Evaluation of the 5F-BAPTA and Nuclear Magnetic Resonance Method as Applied to the Study of Ischemia and Reperfusion , 2005 .

[68]  R. Kloner,et al.  In vivo infusion of oxygen free radical substrates causes myocardial systolic, but not diastolic dysfunction. , 1990, American heart journal.

[69]  N. Dhalla,et al.  Mechanism for depression of heart sarcolemmal Ca2+ pump by oxygen free radicals. , 1989, The American journal of physiology.

[70]  L. Becker,et al.  Alterations in cardiac sarcoplasmic reticulum calcium transport in the postischemic "stunned" myocardium. , 1989, Circulation research.

[71]  R. Bolli,et al.  Direct evidence that oxygen-derived free radicals contribute to postischemic myocardial dysfunction in the intact dog. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[72]  J. Weiss,et al.  Effects of exogenous free radicals on electromechanical function and metabolism in isolated rabbit and guinea pig ventricle. Implications for ischemia and reperfusion injury. , 1989, The Journal of clinical investigation.

[73]  N. Dhalla,et al.  Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals. , 1989, The American journal of physiology.

[74]  R. Kloner,et al.  “Reperfusion Injury” by Oxygen‐Derived Free Radicals?: Effect of Superoxide Dismutase Plus Catalase, Given at the Time of Reperfusion, on Myocardial Infarct Size, Contractile Function, Coronary Microvasculature, and Regional Myocardial Blood Flow , 1989, Circulation research.

[75]  N. Sperelakis,et al.  Myocardial dysfunction and ultrastructural alterations mediated by oxygen metabolites. , 1988, Journal of molecular and cellular cardiology.

[76]  G. Heusch,et al.  Recruitment of inotropic reserve in “stunned” myocardium by the cardiotonic agent AR-L 57 , 1988, Basic Research in Cardiology.

[77]  M. Weisfeldt,et al.  Acidosis during early reperfusion prevents myocardial stunning in perfused ferret hearts. , 1988, The Journal of clinical investigation.

[78]  F. Sheehan,et al.  Early recovery of left ventricular function after thrombolytic therapy for acute myocardial infarction: an important determinant of survival. , 1988, Journal of the American College of Cardiology.

[79]  W. Schaper,et al.  Reversibly Injured, Postischemic Canine Myocardium Retains Normal Contractile Reserve , 1987, Circulation research.

[80]  D. Hearse,et al.  Preconditioning of ischemic myocardium: reperfusion-induced arrhythmias. , 1987, The American journal of physiology.

[81]  R. Kloner,et al.  Diastolic abnormalities of postischemic "stunned" myocardium. , 1987, The American journal of cardiology.

[82]  R. Kerber,et al.  Altered response of reperfused myocardium to repeated coronary occlusion in dogs. , 1987, Journal of the American College of Cardiology.

[83]  L. Becker,et al.  Preserved high energy phosphate metabolic reserve in globally "stunned" hearts despite reduction of basal ATP content and contractility. , 1987, Journal of molecular and cellular cardiology.

[84]  M. Weisfeldt,et al.  Improvement of postischemic myocardial function and metabolism induced by administration of deferoxamine at the time of reflow: the role of iron in the pathogenesis of reperfusion injury. , 1987, Circulation.

[85]  V. Gott,et al.  Free radical scavengers improve functional recovery of stunned myocardium in a model of surgical coronary revascularization. , 1987, Surgery.

[86]  D. Glower,et al.  Dissociation between early recovery of regional function and purine nucleotide content in postischaemic myocardium in the conscious dog. , 1987, Cardiovascular research.

[87]  M. Weisfeldt,et al.  Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts. , 1987, The Journal of clinical investigation.

[88]  C. A. Bailey,et al.  Redox modification of sodium-calcium exchange activity in cardiac sarcolemmal vesicles. , 1986, The Journal of biological chemistry.

[89]  B. Fanburg,et al.  Influence of exogenously generated oxidant species on myocardial function. , 1986, The American journal of physiology.

[90]  P. Serruys,et al.  Effect of coronary occlusion during percutaneous transluminal angioplasty in humans on left ventricular chamber stiffness and regional diastolic pressure-radius relations. , 1986, Journal of the American College of Cardiology.

[91]  D. Warltier,et al.  Beneficial actions of superoxide dismutase and catalase in stunned myocardium of dogs. , 1986, The American journal of physiology.

[92]  R. Kloner,et al.  Superoxide Dismutase Plus Catalase Improve Contractile Function in the Canine Model of the “Stunned Myocardium” , 1986, Circulation research.

[93]  C. Hartley,et al.  Beta-adrenergic stimulation reverses postischemic myocardial dysfunction without producing subsequent functional deterioration. , 1985, The American journal of cardiology.

[94]  R. Sh.  A perspective on the three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. , 1985, Circulation.

[95]  H. Taegtmeyer,et al.  Energy metabolism in reperfused heart muscle: metabolic correlates to return of function. , 1985, Journal of the American College of Cardiology.

[96]  C. Hartley,et al.  Enhancement of recovery of myocardial function by oxygen free-radical scavengers after reversible regional ischemia. , 1985, Circulation.

[97]  J M Nicklas,et al.  Effects of repeated brief coronary occlusion on regional left ventricular function and dimension in dogs. , 1985, The American journal of cardiology.

[98]  J. R. Neely,et al.  Role of Glycolytic Products in Damage to Ischemic Myocardium: Dissociation of Adenosine Triphosphate Levels and Recovery of Function of Reperfused Ischemic Hearts , 1984, Circulation research.

[99]  M. Hess,et al.  Hydrogen peroxide and hydroxyl radical mediation of activated leukocyte depression of cardiac sarcoplasmic reticulum. Participation of the cyclooxygenase pathway. , 1983, Circulation research.

[100]  E. Braunwald,et al.  Studies of experimental coronary artery reperfusion. Effects on infarct size, myocardial function, biochemistry, ultrastructure and microvascular damage. , 1983, Circulation.

[101]  L. Greenfield,et al.  Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers. , 1983, The Journal of thoracic and cardiovascular surgery.

[102]  J. Ross,et al.  Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion. , 1983, Circulation.

[103]  E. Braunwald,et al.  The Stunned Myocardium: Prolonged, Postischemic Ventricular Dysfunction , 1982, Circulation.

[104]  P. Grinwald.  Calcium uptake during post-ischemic reperfusion in the isolated rat heart: influence of extracellular sodium. , 1982, Journal of molecular and cellular cardiology.

[105]  P. McHale,et al.  Prolonged myocardial nucleotide depletion after brief ischemia in the open-chest dog. , 1982, The American journal of physiology.

[106]  Y. Lecarpentier,et al.  Myosin isoenzymic distribution correlates with speed of myocardial contraction. , 1981, Journal of molecular and cellular cardiology.

[107]  R. Jennings,et al.  Prolonged depletion of ATP and of the adenine nucleotide pool due to delayed resynthesis of adenine nucleotides following reversible myocardial ischemic injury in dogs. , 1981, Journal of molecular and cellular cardiology.

[108]  E. Braunwald,et al.  Prolonged derangements of canine myocardial purine metabolism after a brief coronary artery occlusion not associated with anatomic evidence of necrosis. , 1980, Proceedings of the National Academy of Sciences of the United States of America.

[109]  S. Vatner,et al.  Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. , 1975, The Journal of clinical investigation.

[110]  P. F. F. G. R. Heyndrickx M.D..  Hibernating myocardium , 2004, Basic Research in Cardiology.

[111]  R. Bolli,et al.  Effect of adenosine on myocardial 'stunning' in the dog. , 1995, Circulation research.

[112]  R Roberts,et al.  Prolonged abnormalities of left ventricular diastolic wall thinning in the "stunned" myocardium in conscious dogs: time course and relation to systolic function. , 1989, Journal of the American College of Cardiology.

[113]  M. Weisfeldt,et al.  Evidence for a reversible oxygen radical-mediated component of reperfusion injury: reduction by recombinant human superoxide dismutase administered at the time of reflow. , 1987, Circulation.

[114]  S. Rahimtoola.  A perspective on the three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. , 1985, Circulation.