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Time-dependent changes in norepinephrine-induced left ventricular dysfunction and histopathologic condition.

BACKGROUND: Intense activation of the sympathetic nervous system or administration of high concentrations of catecholamines diminishes myocardial contractility and produces infarct-like lesions throughout the heart. This study was conducted to…

Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction.

This study was conducted to determine whether increased myocardial energy demand plays a role in norepinephrine (NE)-induced left ventricular (LV) dysfunction. A range of arterial pressure-heart rate (P-R) products (myocardial energy demand) was…

Temporal changes in left ventricular function after massive sympathetic nervous system activation.

Intense activation of the sympathetic nervous system (SNS) decreases the contractile state of the rabbit left ventricle (LV). In this study, we determined the time course of LV dysfunction after massive central activation of the SNS in dogs.…

Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.

The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to…

Tags: 2016, alpha Subunit/metabolism, American journal of physiology. Heart and circulatory physiology, Amino Acids, Animal, Animals, Apoptosis/drug effects, Cardiotonic Agents/*pharmacology, Cell Hypoxia, Cell Line, Chilian William M, CXCR4/deficiency/genetics/*metabolism, Department of Integrative Medical Sciences, Dicarboxylic/*pharmacology, Disease Models, Dong Feng, Enzyme Inhibitors/pharmacology, Forudi Farhad, hypoxia, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism, Inbred C57BL, Kiedrowski Matthew, Knockout, Left/*drug effects, Mayorga Mari, Mice, myocardial infarction, Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology, Myocardium/*metabolism/pathology, NEOMED College of Medicine, Penn Marc S, Rats, Receptors, Recovery of Function, Shamhart Patricia, Signal Transduction/drug effects, stem cells, Stem Cells/drug effects/metabolism, Stroke Volume/drug effects, Time Factors, Up-Regulation, Ventricular Function, Weber Kristal

Cardiac computed tomographic angiography and the primary care physician.

Through advancements in computer processing speed and storage capacity, new cardiac imaging modalities have become clinically feasible and useful. Cardiac computed tomographic angiography, a new diagnostic imaging modality, is capable of assessing…

Excessive sympathetic nervous system activity decreases myocardial contractility.

The objective of this study was to determine whether myocardial contractility is depressed by intense activation of the sympathetic nervous system. A massive sympathetic discharge was produced by injecting veratrine or sodium citrate into the…

Persistent left ventricular dysfunction after cocaine treatment in rabbits.

The present study was undertaken to determine whether the diminished cardiac performance associated with cocaine administration persists after the drug has been eliminated from the body. Cocaine (5 or 10 mg/kg iv) was administered to conscious (n =…

Role of EDRF in the cardiopulmonary dysfunction produced by massive sympathetic activation.

This study was undertaken to determine whether endothelium-derived relaxing factor (EDRF) modulates the pulmonary and systemic hemodynamic responses to massive sympathetic nervous system (SNS) activation and, in so doing, also modulates the degree of…

Stem Cell Therapy for Heart Disease

Coronary artery disease is the leading cause of death in Americans. After myocardial infarction, significant ventricular damage persists despite timely reperfusion and pharmacological management. Treatment is limited, as current modalities do not…

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