scholarly journals Lymphatic Vessels Mapping in the Lower Extremities of a Healthy Asian Population

2020 ◽  
Vol 25 (3) ◽  
pp. 225-231
Author(s):  
Yun-Hwan Lee ◽  
Hyung-Kyu Kim ◽  
Hi-Jin You ◽  
Deok-Woo Kim
Keyword(s):  
Lymphatic Vessel ◽  
Lymphatic Vessels ◽  
Lower Extremities ◽  
Asian Population ◽  
Skin Incision ◽  
Medial Malleolus ◽  
Lymph Vessels ◽  
Video Images ◽  
Vessel Flow ◽  
Straight Lines

Purpose: Intraoperative indocyanine green (ICG) lymphography is an effective tool to obtain real-time video images of functioning lymph vessels in edematous limbs. However, it is difficult to identify the course of lymph vessels in obese patients or patients with large dermal backflow. Without the image, surgeons have to rely on their experience when performing the skin incision to locate the lymphatic vessels. This study focused on elucidating lymphatic vessel flow patterns in healthy lower extremities in an Asian population to refer these findings for lymphedema treatment.Methods: ICG fluorescence lymphography was performed by injecting 0.2 mL of ICG into the first web space of the foot. After 4 hours, fluorescence images of lymphatic vessels were obtained and the lymphatic vessels were marked. Three landmarks were designated; the medial malleolus, the medial patellar border, and the groin femoral artery. Straight lines connecting the points were drawn, and the distance between the connected lines and the marked lymphatic vessels was measured in eight points. Results: Fifteen subjects with healthy lower extremities (15 right and 15 left) were included. The average course of the main lymph vessels passed 26.2±18.0 mm dorsally to the medial malleolus, 53.7±35.7 mm medially to the medial patellar border, and 25.5±19.2 mm medially to the three-quarters point of the upper landmark line.Conclusion: The main functioning lymphatic vessel largely follows the great saphenous vein course, passes in front of the medial malleolus, runs over the posterior border of the medial epicondyle at the knee level, and travels anteriorly toward the inguinal lymph nodes.

scholarly journals Posttraumatic edema of the lower extremities: Evaluation of the lymphatic vessels with magnetic resonance lymphangiography

2009 ◽  
Vol 49 (2) ◽  
pp. 417-423 ◽  
Author(s):  
Christian Lohrmann ◽  
Gregor Pache ◽  
Gunter Felmerer ◽  
Etelka Foeldi ◽  
Oliver Schaefer ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Lymphatic Vessels ◽  
Lower Extremities

Normal Roentgen Anatomy of the Lymph Vessels of Upper and Lower Extremities

1959 ◽  
Vol Original Series, Volume 51 (5) ◽  
pp. 321-328
Author(s):  
S. Jacobsson ◽  
S. Johansson
Keyword(s):  
Lower Extremities ◽  
Lymph Vessels ◽  
Upper And Lower Extremities

Abstract 27: ApoA-I Improves Lymphatic Function Through a Platelet-Dependent Mechanism in Atherosclerotic Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Andreea Milasan ◽  
François Dallaire ◽  
Gabriel Jean ◽  
Jean-Claude Tardif ◽  
Yahye Merhi ◽  
...  
Keyword(s):  
Lymphatic Vessel ◽  
Ex Vivo ◽  
Lymphatic Vessels ◽  
Lymphatic Transport ◽  
Lv Function ◽  
Experimental Conditions ◽  
Lymphatic Function ◽  
Beneficial Effects ◽  
Dependent Mechanism

Rationale: Lymphatic vessels (LVs) are now recognized as prerequisite players in the modulation of cholesterol removal from the artery wall in experimental conditions of plaque regression, and a particular attention has been brought on the role of the collecting LVs in early atherosclerosis-related lymphatic dysfunction. Whereas recent findings revealed that apoA-I restores the neovascularization capacity of the lymphatic system during tumor necrosis factor-induced inflammation, the effect of apoA-I on collecting LV function during atherosclerosis has not been tested. Objective: In the present study, we address whether and how apoA-I can enhance collecting LV function in atherosclerosis-associated lymphatic dysfunction. Methods and Results: A 6-week systemic treatment with lipid-free apoA-I enhanced lymphatic transport and abrogated collecting lymphatic vessel permeability in atherosclerotic Ldlr –/– mice when compared to control. As injection of apoA-I has been shown to protect wild-type mice against flow restriction-induced thrombosis, and that platelets are identified as key elements in the maintenance of lymphatic vessel integrity via their interaction with lymphatic endothelial cells (LECs), we have tested whether the effects of apoA-I could be mediated through a platelet-dependent mechanism. Our in vivo results show that apoA-I kinetics in lymph reflected that of blood. Ex vivo experiments performed with washed platelets isolated from mouse blood reveal that apoA-I decreased thrombin-induced but not podoplanin-induced platelet aggregation. Whereas this result suggests that apoA-I limits platelet thrombotic potential in blood but not in lymph, we demonstrate that treatment of human LECs with apoA-I increases the adhesion of bridge-like platelets on human LECs. Conclusions: Our results suggest that apoA-I can mediate beneficial effects on lymphatic function by promoting platelet adhesion to the lymphatic endothelium and consequently restore collecting LV integrity. Altogether, we bring forward a new pleiotropic role for apoA-I in lymphatic function and unveil new potential therapeutic targets for the prevention and treatment of atherosclerosis.

scholarly journals The cortical actin network regulates avidity-dependent binding of hyaluronan by the lymphatic vessel endothelial receptor LYVE-1

2020 ◽  
Vol 295 (15) ◽  
pp. 5036-5050 ◽  
Author(s):  
Tess A. Stanly ◽  
Marco Fritzsche ◽  
Suneale Banerji ◽  
Dilip Shrestha ◽  
Falk Schneider ◽  
...  
Keyword(s):  
Lymphatic Vessel ◽  
Leukocyte Adhesion ◽  
Lymphatic Vessels ◽  
Super Resolution ◽  
Direct Interaction ◽  
Correlation Spectroscopy ◽  
Stimulated Emission ◽  
Actin Network ◽  
Cortical Actin ◽  
Limited Mobility

Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) mediates the docking and entry of dendritic cells to lymphatic vessels through selective adhesion to its ligand hyaluronan in the leukocyte surface glycocalyx. To bind hyaluronan efficiently, LYVE-1 must undergo surface clustering, a process that is induced efficiently by the large cross-linked assemblages of glycosaminoglycan present within leukocyte pericellular matrices but is induced poorly by the shorter polymer alone. These properties suggested that LYVE-1 may have limited mobility in the endothelial plasma membrane, but no biophysical investigation of these parameters has been carried out to date. Here, using super-resolution fluorescence microscopy and spectroscopy combined with biochemical analyses of the receptor in primary lymphatic endothelial cells, we provide the first evidence that LYVE-1 dynamics are indeed restricted by the submembranous actin network. We show that actin disruption not only increases LYVE-1 lateral diffusion but also enhances hyaluronan-binding activity. However, unlike the related leukocyte HA receptor CD44, which uses ERM and ankyrin motifs within its cytoplasmic tail to bind actin, LYVE-1 displays little if any direct interaction with actin, as determined by co-immunoprecipitation. Instead, as shown by super-resolution stimulated emission depletion microscopy in combination with fluorescence correlation spectroscopy, LYVE-1 diffusion is restricted by transient entrapment within submembranous actin corrals. These results point to an actin-mediated constraint on LYVE-1 clustering in lymphatic endothelium that tunes the receptor for selective engagement with hyaluronan assemblages in the glycocalyx that are large enough to cross-bridge the corral-bound LYVE-1 molecules and thereby facilitate leukocyte adhesion and transmigration.

scholarly journals Prolonged intake of desloratadine: mesenteric lymphatic vessel dysfunction and development of obesity/metabolic syndrome

2019 ◽  
Vol 316 (1) ◽  
pp. G217-G227 ◽  
Author(s):  
Olga Y. Gasheva ◽  
Irina Tsoy Nizamutdinova ◽  
Laura Hargrove ◽  
Cassidy Gobbell ◽  
Maria Troyanova-Wood ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Side Effects ◽  
Lymphatic Vessel ◽  
Fasting Blood Glucose ◽  
Lymphatic Vessels ◽  
The United States ◽  
Lymph Flow ◽  
The Body

This study aimed to establish mechanistic links between the prolonged intake of desloratadine, a common H1 receptor blocker (i.e., antihistamine), and development of obesity and metabolic syndrome. Male Sprague-Dawley rats were treated for 16 wk with desloratadine. We analyzed the dynamics of body weight gain, tissue fat accumulation/density, contractility of isolated mesenteric lymphatic vessels, and levels of blood lipids, glucose, and insulin, together with parameters of liver function. Prolonged intake of desloratadine induced development of an obesity-like phenotype and signs of metabolic syndrome. These alterations in the body included excessive weight gain, increased density of abdominal subcutaneous fat and intracapsular brown fat, high blood triglycerides with an indication of their rerouting toward portal blood, high HDL, high fasting blood glucose with normal fasting and nonfasting insulin levels (insulin resistance), high liver/body weight ratio, and liver steatosis (fatty liver). These changes were associated with dysfunction of mesenteric lymphatic vessels, specifically high lymphatic tone and resistance to flow together with diminished tonic and abolished phasic responses to increases in flow, (i.e., greatly diminished adaptive reserves to respond to postprandial increases in lymph flow). The role of nitric oxide in this flow-dependent adaptation was abolished, with remnants of these responses controlled by lymphatic vessel-derived histamine. Our current data, considered together with reports in the literature, support the notion that millions of the United States population are highly likely affected by underevaluated, lymphatic-related side effects of antihistamines and may develop obesity and metabolic syndrome due to the prolonged intake of this medication. NEW & NOTEWORTHY Prolonged intake of desloratadine induced development of obesity and metabolic syndrome associated with dysfunction of mesenteric lymphatic vessels, high lymphatic tone, and resistance to flow together with greatly diminished adaptive reserves to respond to postprandial increases in lymph flow. Data support the notion that millions of the USA population are highly likely affected by underevaluated, lymphatic-related side effects of antihistamines and may develop obesity and metabolic syndrome due to the prolonged intake of this medication.

scholarly journals S1P-S1PR1 activity controls VEGF-A signaling during lymphatic vessel development

2019 ◽  
Author(s):  
AM Golding-Ochsenbein ◽  
S Vidal ◽  
B Wilmering Wetter ◽  
C Guibourdenche ◽  
C Beerli ◽  
...  
Keyword(s):  
Lymphatic Vessel ◽  
Lymphatic Vessels ◽  
Signaling Crosstalk ◽  
Balanced Growth ◽  
Sphingosine 1 Phosphate ◽  
Genetic Deletion ◽  
Vessel Development ◽  
Perinuclear Area

AbstractSphingosine-1-phosphate (S1P), a lipid signaling molecule produced by endothelial cells, is required for development and homeostasis of blood vessels. However, its role during lymphatic vessel development is unclear. We show in murine newborns that pharmacologically enhanced S1P signaling increases VEGF-A-dependent LEC proliferation. In contrast, S1PR1 inhibition, mediated by the antagonist NIBR0213 or LEC-specific genetic deletion of S1pr1, promotes filopodia formation and vessel branching, independent of VEGF-A. To investigate the S1P and VEGF-A signaling crosstalk observed in vivo, we used LECs cultured in vitro. We demonstrate that S1P activates endogenous S1PR1 in a constitutive, autocrine manner. Importantly, S1P-S1PR1 activity was required for VEGF-A-induced LEC proliferation and strongly supported ERK1/2 activation and VEGFR-2 trafficking to the perinuclear area. In conclusion, S1P-S1PR1 signaling promotes VEGF-A-dependent LEC proliferation and limits migratory and filopodia-forming responses. Hence, S1P-S1PR1 signaling is required for balanced growth factor-induced lymphangiogenesis and correctly patterned lymphatic vessels during postnatal development.

scholarly journals Nano-engineered VEGF-C ameliorates gut lymphatic drainage, portal pressure and ascites in experimental portal hypertension

2020 ◽  
Author(s):  
Savneet Kaur ◽  
Dinesh M Tripathi ◽  
Pinky Juneja ◽  
Impreet Kaur ◽  
Sumati Rohilla ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Portal Hypertension ◽  
Lymphatic Vessel ◽  
Lymphatic Vessels ◽  
Lymphatic Drainage ◽  
List Type ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
Compensated Cirrhosis ◽  
Endothelial Growth Factor

AbstractObjectiveGut lymphatic vessels are crucial in maintaining abdominal fluid homeostasis. We studied these vessels in clinical cirrhosis and explored effects of vascular endothelial growth factor-C (VEGF-C), a pro-lymphangiogenic factor, in experimental portal hypertension.DesignVascular endothelial growth factor receptor 3 (vegfr3)-positive lymphatic channels were enumerated in duodenal (D2) biopsies from cirrhotic patients. Vegfr3 antibody-tagged lipid nanocarriers were used to formulate novel nano-engineered (E-VEGF-C) molecule for targeted lymphangiogenesis of gut lymphatic vessels. The uptake of E-VEGF-C was evaluated in lymphatic endothelial cells (LyECs) in vitro and in vivo. The effects of E-VEGF-C were tested in cirrhotic and non-cirrhotic animal models of portal hypertension. Animals given nanocarriers alone served as vehicle. Mesenteric lymphatic vessel numbers/proliferation and drainage were analyzed. Abdominal ascites, hepatic and systemic hemodynamics was measured. Liver, duodenum, mesentery and plasma were examined.ResultsIn D2 biopsies, number of dilated vegfr3+ lymphatic vessels was significantly increased in decompensated as compared to compensated cirrhosis and correlated with presence of ascites. E-VEGF-C was efficiently taken up by the mesenteric LyECs. E-VEGF-C treated rats displayed a marked increase in the proliferation of mesenteric lymphatic vessels and drainage as compared to CCl4-vehicle. Ascites and mesenteric inflammation were markedly reduced in E-VEGF-C treated cirrhotic rats. Portal pressures were attenuated in both cirrhotic and non-cirrhotic portal hypertensive rats treated with E-VEGF-C as compared to respective vehicle groups.ConclusionE-VEGF-C molecule enhances mesenteric lymphangiogenesis and improves lymphatic vessel drainage, attenuating abdominal ascites and portal pressures. Targeted gut lymphangiogenesis may serve as an emerging therapy for portal hypertension.Significance of the StudyWhat is already known about this subject?Gut lymphatic vessels play crucial roles in maintaining fluid and immune homeostasis in the abdomen.An increased but dysfunctional gut lymphangiogenesis occurs to compensate for lymphatic insufficiency in patients with gut inflammatory diseases.Therapies aimed at enhancing lymphangiogenesis with growth factors such as VEGF-C constitute an effective strategy to improve lymphatic drainage and ameliorate inflammation in certain pathologies.Gut lymphatic vessels remain poorly characterized in patients with cirrhosis.What are the new findings?Dilated vegfr3+ lymphatic vessels are significantly increased in patients with decompensated as compared to compensated cirrhosis and correlated with presence of ascites.A nanoengineered pro-angiogenic molecule, E-VEGF-C with specificity for uptake by the gut lymphatic endothelial cells molecule enhances mesenteric lymphangiogenesis.E-VEGF-C improved lymphatic vessel drainage, attenuating abdominal ascites and portal pressures.How might it impact on clinical practice in the foreseeable future?Gut lymphangiogenesis is proposed as an innovative strategy for the management of ascites and portal hypertension.

scholarly journals Comparison of normal hindlimb lymphatic systems in rats with detours present after lymphatic flow blockage

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260404
Author(s):  
Yuiko Suzuki ◽  
Yukari Nakajima ◽  
Toshio Nakatani ◽  
Mayumi Okuwa ◽  
Junko Sugama
Keyword(s):  
Lymph Node ◽  
Lymphatic Vessel ◽  
Near Infrared ◽  
Imaging System ◽  
Lymphatic Vessels ◽  
Lymphatic Drainage ◽  
Lymphatic Flow ◽  
Fluorescence Imaging System ◽  
Normal Rat ◽  
Flow Blockage

In the present study, we aimed to identify the normal hindlimb lymphatic systems in rats and compare them with the detours after lymphatic flow blockage. The lymphatic systems of the hindlimbs of normal rats were investigated via lymphography using a near-infrared fluorescence imaging system. The lymphatic vessels were stained using Evans Blue. The lymphatic flow was blocked through lymphatic vessel ligation combined with inguinal and popliteal lymph node dissection. Detours that appeared after 30 days were visualized using lymphography and immunostaining with anti-podoplanin antibodies. Three main results were obtained in the present study. First, the deep medial system, the superficial medial system, a connection between the superficial and deep medial lymphatic systems, and the superficial lateral system, were elucidated. Second, three types of detours, namely the detour of the lateral abdomen, the detour to the lymphatic vessel near the midline of the abdomen, and the detour to the contralateral inguinal lymph node, were identified after lymphatic flow blockage. Lastly, detours were located in the fatty layer above the panniculus carnosus muscle and their lumina were wide. The histology suggested that the detour was a pre-collecting lymphatic vessel. Lymphatic routes in the rat hindlimbs after lymphatic flow blockage were different from those of the normal rat lymphatic system. It was suggested that the detour is a pre-collecting lymphatic vessel and that encouraging its development may be a new method of simple lymphatic drainage.

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