Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts.
about
Ca2+ Sparks and Ca2+ waves are the subcellular events underlying Ca2+ overload during ischemia and reperfusion in perfused intact hearts.Comparison of human induced pluripotent stem-cell derived cardiomyocytes with human mesenchymal stem cells following acute myocardial infarctionTransient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion.Brief rapid pacing depresses contractile function via Ca(2+)/PKC-dependent signaling in cat ventricular myocytes.Calcium and the anaesthetist.Activity of the Na+/H+ exchanger contributes to cardiac damage following ischaemia and reperfusion.Rapid expression of heat shock protein in the rabbit after brief cardiac ischemia.Calcium oscillations index the extent of calcium loading and predict functional recovery during reperfusion in rat myocardium.Intracellular free calcium concentration measured with 19F NMR spectroscopy in intact ferret heartsRelationship between ionic perturbations and electrophysiologic changes in a canine Purkinje fiber model of ischemia and reperfusionAcidosis during early reperfusion prevents myocardial stunning in perfused ferret heartsEffects of exogenous free radicals on electromechanical function and metabolism in isolated rabbit and guinea pig ventricle. Implications for ischemia and reperfusion injury.Relationship between calcium loading and impaired energy metabolism during Na+, K+ pump inhibition and metabolic inhibition in cultured neonatal rat cardiac myocytes.Structure of the NH2-terminal variable region of cardiac troponin T determines its sensitivity to restrictive cleavage in pathophysiological adaptationTriple threat: the Na+/Ca2+ exchanger in the pathophysiology of cardiac arrhythmia, ischemia and heart failure.An inhibitor of poly (ADP-ribose) synthetase activity reduces contractile dysfunction and preserves high energy phosphate levels during reperfusion of the ischaemic rat heart.Sustained left ventricular diastolic dysfunction after exercise in patients with dilated cardiomyopathy.Extracellular Adenosine Formation by Ecto-5'-Nucleotidase (CD73) Is No Essential Trigger for Early Phase Ischemic PreconditioningBeneficial effects of N-acetylcysteine and cysteine in stunned myocardium in perfused rat heart.The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping.The importance of the Thr17 residue of phospholamban as a phosphorylation site under physiological and pathological conditions.New concepts of endoplasmic reticulum function in the heart: programmed to conserve.Early reperfusion phenomena.Ischemia-reperfusion and cardioprotection: a delicate balance between reactive oxygen species generation and redox homeostasis.Post-resuscitation hemodynamics and relationship to the duration of ventricular fibrillation.A cardioprotective role for platelet-activating factor through NOS-dependent S-nitrosylationTargeting calcium transport in ischaemic heart disease.Effects of inotropic drugs on mechanical function and oxygen balance in postischemic canine myocardium: comparison of dobutamine, epinephrine, amrinone, and calcium chloride.Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy.Calcium and pH in anoxic and toxic injury.Is the protection against ischemia induced by red wine linked to its antioxidant capacity?Carbon monoxide increases inducible NOS expression that mediates CO-induced myocardial damage during ischemia-reperfusion.Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury.Creatine kinase-deficient hearts exhibit increased susceptibility to ischemia-reperfusion injury and impaired calcium homeostasis.Depressed tolerance to fluorocarbon-simulated ischemia in failing myocardium due to impaired [Ca(2+)](i) modulation.Preservation of metabolic reserves and function after storage of myocytes in hypothermic UW solution.Na(+)/H(+) exchange subtype 1 inhibition reduces endothelial dysfunction in vessels from stunned myocardium.Changes in excitation-contraction coupling in an isolated ventricular myocyte model of cardiac stunning.Role of dual-site phospholamban phosphorylation in the stunned heart: insights from phospholamban site-specific mutants.Evidence of myofibrillar protein oxidation induced by postischemic reperfusion in isolated rat hearts.
P2860
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P2860
Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts.
description
1987 nî lūn-bûn
@nan
1987 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
1987 թվականի մարտին հրատարակված գիտական հոդված
@hy
1987年の論文
@ja
1987年論文
@yue
1987年論文
@zh-hant
1987年論文
@zh-hk
1987年論文
@zh-mo
1987年論文
@zh-tw
1987年论文
@wuu
name
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@ast
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@en
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@nl
type
label
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@ast
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@en
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@nl
prefLabel
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@ast
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@en
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@nl
P2093
P2860
P356
P1476
Pathophysiology and pathogenes ...... ium overload in ferret hearts.
@en
P2093
H F Weisman
J K Porterfield
M L Weisfeldt
P2860
P304
P356
10.1172/JCI112906
P407
P577
1987-03-01T00:00:00Z