Mechanical function, glycolysis, and ultrastructure of perfused working mouse hearts following thoracic aortic constriction
| Autor: | Arthur C. Cosmas, Frederick J. Vetter, Thomas G. Manfredi, Michael E. Dunn, Joshua N. King, Robert L. Rodgers |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Cardiac output medicine.medical_specialty Time Factors Systole Biopsy Diastole Aorta Thoracic Biology Left ventricular hypertrophy Ventricular Function Left Pathology and Forensic Medicine Muscle hypertrophy Mice Ventricular Dysfunction Left Microscopy Electron Transmission medicine.artery Internal medicine medicine Ventricular Pressure Animals Cardiac Output Ventricular remodeling Ligation Aorta Ventricular Remodeling Myocardium General Medicine medicine.disease Fibrosis Mice Inbred C57BL Perfusion Disease Models Animal Cardiology Ventricular pressure Hypertrophy Left Ventricular Cardiology and Cardiovascular Medicine Glycolysis |
| Zdroj: | Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. 20(6) |
| ISSN: | 1879-1336 |
| Popis: | Background: Glycolytic flux in the mouse heart during the progression of left ventricular hypertrophy (LVH) and mechanical dysfunction has not been described. Methods: The main objectives of this study were to characterize the effects of thoracic aortic banding, of 3- and 6-week duration, on: (1) left ventricular (LV) systolic and diastolic function of perfused working hearts quantified by analysis of pressure– volume loops; (2) glycolytic flux in working hearts expressed as the rate of conversion of 3 H-glucose to 3 H2O, and (3) ultrastructure of LV biopsies assessed by quantitative and qualitative analysis of light and electron micrographs. Results: Results revealed that (1) indexes of systolic function, including LV end-systolic pressure, cardiac output, and rate of LV pressure development and decline, were depressed to similar degrees at 3 and 6 weeks post-banding; (2) diastolic dysfunction, represented by elevated LV end-diastolic pressure and volume, was more severe at 6 than at 3 weeks, consistent with a transition to failure; (3) a progressive decline in glycolytic flux that was roughly half the control rate by 6 weeks post-banding; and (4) structural derangements, manifested by increases in interstitial collagen content and myocyte Z-band disruption, that were more marked at 3 weeks than at 6 weeks. Conclusion: The results are consistent with the view that myocyte damage, fibrosis, and suppressed glycolytic flux represent maladaptive structural and metabolic remodeling that contribute to the development of failure in high pressure load-induced LVH in the mouse. Published by Elsevier Inc. |
| Databáze: | OpenAIRE |
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