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Updated: May 28, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Increased collagen, per se, may not affect left ventricular function in spontaneously hypertensive rats
Dinko Susic1, Edward D Frohlich
1Hypertension Research Laboratory, Division of Research, Ochsner Clinic Foundation, New Orleans, LA.
Moderate left ventricular fibrosis, induced by inhibiting matrix metalloproteinases, did not impair cardiac function in hypertensive rats. This suggests other collagen changes, not just accumulation, cause fibrosis-related cardiac dysfunction.
Area of Science:
- Cardiovascular Research
- Cardiac Fibrosis
- Matrix Metalloproteinase Inhibition
Background:
- Left ventricular fibrosis is a key factor in cardiac dysfunction.
- Quantifying fibrosis's role is challenging due to concurrent myocyte and vascular changes.
- Matrix metalloproteinase (MMP) inhibitors can induce collagen accumulation.
Purpose of the Study:
- To investigate the specific role of myocardial fibrosis in cardiac dysfunction.
- To determine if doxycycline-induced collagen accumulation affects cardiac function.
- To isolate the impact of fibrosis from other pathological changes.
Main Methods:
- Adult male spontaneously hypertensive rats were used.
- One group received doxycycline (MMP inhibitor) for 6 months; a control group received no treatment.
- Cardiac function, arterial pressure, aortic stiffness, and myocardial collagen were assessed.
Main Results:
- Doxycycline treatment significantly increased ventricular collagen concentration.
- Arterial pressure and aortic stiffness remained unchanged.
- Left ventricular function, including dP/dt and diastolic time constant, was unaffected.
Conclusions:
- Moderate collagen accumulation alone does not adversely affect cardiovascular function.
- Other collagen modifications, such as advanced glycation end-products, may drive fibrosis-related dysfunction.
- This study helps differentiate the direct impact of fibrosis on cardiac health.
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