Changes of Thoracic Duct Flow and Morphology in an Animal Model of Elevated Central Venous Pressure
Highlights
- The TD is the largest lymphatic vessel in the body and transports the majority of the lymph in the body except for the head, neck, arm, and right thorax in humans (View Highlight)
- Approximately 50 years ago, it was shown that there is no capillary venous reabsorption of interstitial fluid, revealing that the lymphatic system is solely responsible for the removal of interstitial fluid (View Highlight)
- Elevations of CVP in CHF affect the lymphatic system in two ways: 1) increased lymph production due to increased plasma ultrafiltration from the capillary bed into interstitial tissue, especially in the liver portal circulation (Dumont et al., 1963; Wegria et al., 1963; Cole et al., 1967; Szabo and Magyar, 1967; Witte et al., 1969; Kusaka et al., 2003; Dib et al., 2006; Shimizu, 2008); and 2) increased TD afterload pressure at the lymphovenous junction which impedes TD flow (View Highlight)
- The dramatic, rapid, and sustained increase in TDQ following induction of severe TR indicates that increased lymph production is the dominant factor. (View Highlight)
- Although the enlargement of the TD may reduce the resistance to flow (Poiseuille’s law), it may cause insufficiency of the lymphatic valve leaflets due to loss of coaptation (View Highlight)
- Lymphatic valve insufficiency may cause a negative spiral of lymphatic failure where valve failure causes further volume-overload which further dilates TD and exacerbates valve function, and so on. (View Highlight)
- increased flow or wall shear stress induces diameter enlargement (outward remodeling) of arteries and veins (View Highlight)
- increased pressure results in significant arterial remodeling (wall thickening) to restore wall stress to homeostasis (View Highlight)
- central venous pressure affects lymphatic production more than impedes lymphatic flow as the primary mechanism in the formation of interstitial edema (View Highlight)
- This increased flow results in the TD remodeling, i.e., increased TD diameter as well as increased wall thickness. The TD wall thickening offsets the increase in circumferential wall stress. However, the insufficient outward remodeling of the TD only partially counteracts the elevations of shear stress. Although the outward remodeling of the TD can eventually restore the wall shear stress levels, it can result in TD valve incompetence due to failure coaptation of valvular leaflets, as demonstrated by negative lymph flows (View Highlight)