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Published on: June 14, 2016
Pathogenesis of myocardial fibrosis in spontaneously hypertensive rats (SHR)
H J Herrmann1, U Fiedler, R Blödner
1Max Delbrück Centre of Molecular Medicine, Berlin, Germany.
Insights
Myocardial fibrosis mechanisms in spontaneous hypertension involve coronary microvessel changes. Early hypertension shows reduced microvessels and fibrosis, while later stages reveal increased microvessels and distinct fibrosis patterns.
Area of Science:
- Cardiovascular pathology
- Hypertension research
- Fibrosis mechanisms
Background:
- Pathomechanisms of myocardial fibrosis remain unclear.
- Spontaneous hypertensive rats (SHR) serve as a model for studying hypertension-induced cardiac changes.
- Morphological alterations in coronary microvessels (MV) and myocardial lesions are implicated in fibrosis.
Purpose of the Study:
- To investigate the role of coronary microvessels and interstitial reactions in the development of myocardial fibrosis in SHR.
- To differentiate the pathomechanisms of fibrosis during the developing and manifest phases of spontaneous hypertension.
- To elucidate the relationship between microvascular changes and myocardial lesions in hypertensive hearts.
Main Methods:
- Utilized novel morphological preparations and measurement techniques.
- Examined myocardial tissue from SHR and control rats across various age points (3, 13, 27, 52, 78 weeks).
- Quantified numerical and area densities of coronary microvessels and fibrotic tissue.
Main Results:
- Developing phase of SH (up to 13 weeks): Lower MV and fibrotic tissue density compared to controls.
- Manifest phase of SH (27-78 weeks): Increased MV and fibrotic tissue density.
- Pathological MV reactions, representing chronic contractions, correlate with interstitial tissue increase.
- Early manifest phase (27-52 weeks): Generalized myocardial fibrosis.
- Late manifest phase (52-78 weeks): Localized fibrosis linked to focal ischemic lesions, excluding the septal region.
Conclusions:
- Myocardial fibrosis development in SHR is linked to microvascular alterations.
- Distinct pathomechanisms underlie fibrosis in the developing versus manifest phases of spontaneous hypertension.
- Small, often undetected microvessels play a crucial role in hypertensive cardiac remodeling and fibrosis.
Abstract:
The pathomechanisms of myocardial fibrosis are incompletely understood. Coronary microvessels (MV), interstitial reactions and focal myocardial lesions characterized by morphological signs of ischaemia were found in 39 spontaneous hypertensive rats (SHR) and 33 control rats aged 3, 13, 27, 52 and 78 weeks, using new morphological preparations and measuring methods. In the developing phase of spontaneous hypertension (SH) the numerical and area densities (developed for up to 13 weeks) of MV were lower than at 3 weeks and lower than control. The same was true for the fibrotic tissue density. However, all values were increased in the manifest phase of SH (27-78 weeks). The increase in interstitial tissue is topologically and causally related to pathological MV reactions that represent morphologically chronically increased contractions. Small MV that mostly elude detection with conventional staining methods are of particular importance. The first phase of manifest SH (27th-52nd week) is characterized by a generalized development of myocardial fibrosis; the late phase (52nd-78th week) by a reinforced localized fibrosis that is attributable to the enhanced progression of focal ischaemic myocardial lesions. The septal region is not included in this phase. Thus, in the two phases of manifest SH, the pathomechanisms responsible for the development of myocardial fibrosis must be different.
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