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Fine structure of capillary proliferation in myocardium of volume overloaded rats
K Kawamura1, K Tohda, M Kobayashi
12nd Department of Pathology, Akita University School of Medicine, Japan.
Insights
Cardiac hypertrophy induced by volume overload leads to increased capillary endothelial cell proliferation in rat hearts. This suggests increased coronary blood flow drives endothelial cell changes.
Area of Science:
- Cardiovascular Biology
- Cell Biology
- Physiology
Background:
- Cardiac hypertrophy is a significant cardiovascular adaptation.
- Understanding the microvascular response is crucial for cardiac health.
- Volume overload models are used to study cardiac remodeling.
Purpose of the Study:
- To investigate the fine structure of capillary endothelial cells in volume-overloaded cardiac hypertrophy.
- To determine the timeline of endothelial cell changes in response to sustained volume overload.
Main Methods:
- Utilized an arteriovenous (A-V) shunt model in rats to induce volume overload.
- Examined intramyocardial capillaries using transmission electron microscopy (TEM).
- Quantified endothelial cell numbers and observed structural changes at 1, 2, and 4 weeks post-shunt.
Main Results:
- Significant increases in left ventricle volume and weight were observed.
- Endothelial cell activation was noted as early as 1 week.
- Proliferation (over 3 cells/capillary) and structural changes (bulging, overlapping, increased microvilli) were prominent at 2 weeks.
Conclusions:
- Volume overload triggers rapid activation and proliferation of capillary endothelial cells in the heart.
- Increased coronary blood flow is a likely stimulus for endothelial proliferation.
- Capillary lumen dilatation may regulate these adaptive changes.
Abstract:
We studied the fine structure of capillary endothelial cells of volume over-loaded cardiac hypertrophy in rats using A-V shunt between the left common carotid artery and the left external jugular vein. The duration of experiment was 1, 2 and 4 weeks. Volume overload of the heart was constantly induced, because blood flow index (ml/min/kg) of both carotid arteries was increased throughout the experiment and the volume and the weight of the left ventricle were significantly increased in 2 and 4 weeks. After the making of the large panorama photograph composed of 24 TEM photographs, the number of the endothelial cells of each capillary was directly counted under TEM. In 2-week shunted animals, incidences of over 3 endothelial cells per capillary were definitely increased. Also bulging of the endothelial cells, overlapping of two endothelial cells and increasing of microvilli on the luminal surface were mostly prominent in 2 weeks. Endothelial cells of intramyocardial capillaries are considered to be activated as early as 1 week and proliferated in around 2 weeks after volume-overload. An increase of coronary blood flow might be one of the most important causes of the endothelial proliferation and regulated by dilatation of the capillary lumen.