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Changes in extracellular collagen matrix alter myocardial systolic performance
Catalin F Baicu1, Jason D Stroud, Virginia A Livesay
1Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston 29401, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|December 18, 2002
Summary
Disrupting fibrillar collagen in heart muscle significantly impairs systolic performance. However, individual heart cell contractility remains unchanged, suggesting collagen
Area of Science:
- Cardiovascular Biology
- Extracellular Matrix Research
- Cardiac Physiology
Background:
- The extracellular matrix, particularly fibrillar collagen, plays a critical role in cardiac structure and function.
- Understanding the specific contribution of collagen to myocardial mechanics is essential for comprehending heart disease.
- Previous research suggests collagen influences force transmission but direct evidence is limited.
Purpose of the Study:
- To investigate the impact of acute disruption of fibrillar collagen on myocardial systolic performance.
- To determine if collagen degradation affects cardiomyocyte contractility independently of overall heart muscle function.
- To test the hypothesis that fibrillar collagen is crucial for translating cardiomyocyte contraction into effective myocardial force.
Main Methods:
- Isolated papillary muscles from animal models were treated with plasmin to induce collagen degradation.
- Gelatin zymography, hydroxyproline assays, and scanning electron microscopy were used to confirm collagen degradation and matrix metalloproteinase activation.
- Myocardial systolic performance was assessed by measuring isotonic shortening extent and isometric developed tension.
- Cardiomyocyte contractility was evaluated by measuring shortening extent and velocity in isolated cells.
Main Results:
- Plasmin treatment led to significant collagen degradation and matrix metalloproteinase activation.
- Myocardial systolic performance decreased significantly, with reduced isotonic shortening extent and isometric developed tension.
- Isolated cardiomyocyte contractility (shortening extent and velocity) was not altered by plasmin treatment.
- A significant reduction in myocardial systolic performance was observed following acute collagen disruption.
Conclusions:
- Acute disruption of the fibrillar collagen network significantly impairs myocardial systolic performance.
- Fibrillar collagen is essential for the effective transduction of cardiomyocyte contraction into myocardial force.
- These findings highlight the mechanical role of the extracellular matrix in maintaining normal cardiac systolic function.
- The study supports the hypothesis that fibrillar collagen is vital for myocardial performance, independent of individual cardiomyocyte contractility.
Keywords:
Non-programmatic