Key result
Hypertension in Dahl S rats induced extensive cardiac lymphatic fibrosis and ultrastructural changes in the lymphatic endothelium compared to Dahl R controls.
Why the study?
Does hypertension cause ultrastructural changes in the cardiac lymphatic system in a rat model?
Does hypertension cause ultrastructural changes in the cardiac lymphatic system in a rat model?
Hypertension induces significant structural changes and fibrosis in cardiac lymphatics, highlighting them as a potential therapeutic target for hypertensive heart disease.
Cardiac lymphatic fibrosis may offer a novel target in hypertensive heart disease; hypothesis-generating in this rat model and leaves clinical translation open.
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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Li et al. (2009) studied Hypertension. Hypertension (Dahl S rats) vs. Dahl R rats (control group) was evaluated on Ultrastructural changes in cardiac lymphatics and expression of collagen fibers, atrial natriuretic peptide, connexin43, and LYVE-1. Hypertension in Dahl S rats induced extensive cardiac lymphatic fibrosis and ultrastructural changes in the lymphatic endothelium compared to Dahl R controls.
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