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Ultrastructure changes of cardiac lymphatics during cardiac fibrosis in hypertensive rats
Xiaodong Li1, Tatsuo Shimada, Yafang Zhang
1Department of Anatomy, Harbin Medical University, Harbin, China.
Insights
Hypertension causes cardiac lymphatic fibrosis, with structural changes potentially contributing to heart disease. Targeting cardiac lymphatics may offer new treatments for hypertension-induced fibrosis.
Area of Science:
- Cardiovascular Biology
- Lymphatic System Research
- Pathology
Background:
- Hypertension induces significant pathological changes in organs, particularly the heart.
- While cardiac blood vessels in hypertension are well-studied, cardiac lymphatic system structural changes remain largely unknown.
Purpose of the Study:
- To investigate the structural alterations within the cardiac lymphatic system during hypertension.
- To determine the role of cardiac lymphatic system changes in the development of cardiac fibrosis associated with hypertension.
Main Methods:
- Developed a hypertension animal model using Dahl S rats, with Dahl R rats as controls.
- Utilized immunohistochemistry to examine collagen fibers, atrial natriuretic peptide, connexin43, and LYVE-1 expression.
- Employed transmission electron microscopy and scanning electron microscopy to analyze cardiac lymphatic ultrastructure.
Main Results:
- Observed extensive lymphatic fibrosis in hypertensive rat hearts, marked by increased thin collagen fibrils directly interacting with lymphatics.
- Identified ultrastructural changes in cardiac lymphatic endothelium, including increased vesicles, vacuoles, active exocytosis, and cytoplasmic processes.
- These endothelial changes appeared to facilitate the draining of tissue fluid.
Conclusions:
- Structural changes in the cardiac lymphatic system are implicated as a significant factor in cardiac fibrosis during hypertension.
- The cardiac lymphatic system presents a potential therapeutic target for mitigating fibrosis in hypertension treatment.
Abstract:
Hypertension is one of the most common diseases that induce a series of pathological changes in different organs of the human body, especially in the heart. There is a wealth of evidence about blood vessels in hypertensive myocardium, but little is known about structural changes in the cardiac lymphatic system. To clarify the changes in structure of the cardiac lymphatic system during hypertension, we developed a hypertension animal model with Dahl S rats and we used Dahl R rats as the control group. We examined the expression of collagen fibers, atrial natriuretic peptide, connexin43, and LYVE-1 in the rat heart by immunohistochemistry. The ultrastructure of the cardiac lymphatics was detected by transmission electron microscopy and scanning electron microscopy. We demonstrated extensive lymphatic fibrosis in the hearts of the Dahl S hypertension group, characterized by increased thin collagen fibrils that connected with the lymphatics directly. Ultrastructural changes in the cardiac lymphatic endothelium such as an increase of vesicles and occurrence of vacuoles, active exocytosis, and cytoplasmic processes, restored the draining of tissue fluid. Our study suggests that during hypertension, the changes in structure of the cardiac lymphatics may be one important factor involved in cardiac fibrosis. Therefore, the lymphatics may be a possible target for reducing fibrosis in the treatment of hypertension.
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