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PubMedDate not supplied

[Direct and prolonged effect of thyroliberin in ultra small doses on contractility of the white rat mesentery lymphatic vessels].

The prolonged effect of thyroliberin in ULD after single intramuscular injection on contractility of lymphatic vessels directly was investigated. The controlled group of animals received injection of 0.2 ml of physiological solution. The experimental group was injected by 0.2 ml of thyroliberin in concentrations of 10(-10) or 10(-16) mol/l (1 x 10(-4) and 1 x 10(-10) micrograms/kg of the body weight respectively). During the experiment the animals were grouped in the following way: 1) directly after the injection; 2) 3 hours later; 3) on the 1st day and then every day during 2 weeks. Lymphatic vessels reactivity of the experimental animals as well as controlled was studied by application of thyroliberin and noradrenalin (in concentrations of 1 x 10(-16) and 1 x 10(-6) mol/l respectively) directly on mesentery lymphatic vessels. The lymphatic vessels reaction in control group of animals on the noradrenalin and thyroliberin was the same during the period of observation. Thyroliberin stimulated contractility at concentration of 1 x 10(-16) mol/l. The reaction of experimental group was dramatically decreased to 10(-4) mol/l on the 1st and the 3rd day (in the case i.m. injected concentration 1 x 10(-10) mol/l) and to 10(-10) mol/l (in the case of i.m. injected concentration 10(-16) mol/l). The lymphatic vessels reactivity to exogenous thyroliberin gradually established at the 6-7th days till 12th day from the moment of thyroliberin injection. The mechanisms of the action of thyroliberin in ULD are discussed.

Animals↗

PubMed2004

Proliferation of D2-40-expressing intestinal lymphatic vessels in the lamina propria in inflammatory bowel disease.

Lymphatic vessels in the colon are normally distributed beneath the muscularis mucosae with rare branches reaching through the muscularis mucosae to the most basal aspect of the colonic crypts. In chronic inflammatory bowel disease demonstrating acute inflammation and architectural disarray, lymph vessel proliferation is seen within the lamina propria and within the submucosa. We analyzed the number and distribution of lymphatic vessels within the lamina propria and submucosa in chronic active and treated ulcerative colitis with restoration of architecture by immunostaining with D2-40, a specific monoclonal antibody against lymphatic vessels. We found significantly increased numbers of lymph vessels in chronic active ulcerative colitis both within the lamina propria and the submucosa as compared to normal mucosa. Numbers of lymph vessels in lamina propria were highest in severe chronic active ulcerative colitis and less in moderate and minimal residual disease with minimal architectural disarray (p<0.05). Lymph vessels in the submucosa were increased significantly above normal values in both severe, moderate and minimal residual disease. We conclude that lymph vessel distribution in chronic active ulcerative colitis extends into the lamina propria. With restoration of architectural morphology, the integrity of the lamina propria in regards to the distribution of lymph vessels is restored.

Antibodies, Monoclonal↗

PubMed1992

Intestinal lymphatic vessels release endothelial-dependent vasodilators.

This study evaluated the possibility that the endothelial cells of microscopic lymphatic vessels can release vasoactive agents which affect the lymphatic vessels and nearby arterioles. Microinotophoresis of acetylcholine (ACh) or bradykinin (BK) onto the wall of quiescent submucosal lymphatic vessels in the rat small intestine had no discernible effects on their diameters but caused spontaneously active mesenteric lymphatic vessels to constrict. Application of ACh or BK to the arteriolar wall caused significant vasodilation. Release of either drug onto the wall of a nearby lymphatic produced arteriolar dilation that was approximately 80% of that observed with direct application to the arteriolar wall; drug application into parenchymal tissue produced a dilation less than 25% of that observed during application to the lymphatic. NG-monomethyl-L-arginine application to the lymphatic blocked all ACh-induced lymphatic-mediated responses but had no effect on the response to direct ACh application to the arteriolar wall or any of the responses to BK application. These results are consistent with the hypothesis that lymphatic endothelial cells are capable of releasing agents that dilate nearby arterioles and cause spontaneously active lymphatic vessels to constrict.

Acetylcholine↗

PubMed2006

Distribution of lymphatic vessels in the neural plexuses surrounding the superior mesenteric artery.

OBJECTIVES: To investigate whether lymphatic vessels exist in the neural plexuses surrounding the superior mesenteric artery (SMA) and the ultrastructural relationship between neural plexuses and lymphatic vessels. METHODS: A total of 970 serial sections including the structure surrounding the SMA were obtained from 9 cadavers. They were subjected to conventional hematoxylin/eosin staining and immunostaining for the lymphatic marker D2-40. Epithelial membrane antigen and S100 were also immunostained to identify the perineurium and nerve bundles, respectively. RESULTS: Thin-walled, erythrocyte-free vessels staining with lymphatic markers (D2-40) were found in the neural plexuses surrounding the SMA along a full circumference. There seemed to be a distribution correlation between lymphatic vessels and neural plexuses. Lymphatic vessels were not identified within the nerve bundles. The plexuses contained no lymph nodes in any sections. CONCLUSIONS: To our knowledge we report the immunohistochemical visualization of lymphatic vessels in peri-SMA neural plexuses for the first time. Therefore, particular attention should be paid to the lymphatic vessels within neural plexuses as a possible route of invasion and the source of pancreatic cancer recurrence.

Aged↗

PubMed2002

Effects of histamine on the contractile and electrical activity in isolated lymphatic vessels of the guinea-pig mesentery.

1 The effect of histamine on the rate of lymphatic vessel constrictions and lymphatic smooth muscle membrane potential was examined in the guinea-pig mesentery. 2 Histamine (0.01-5 micro M) increased the frequency and decreased the amplitude of constrictions in lymphatic vessels under intraluminal perfusion. This response was accompanied by a depolarization of the smooth muscle membrane potential, an increase in the activity of spontaneous transient depolarizations (STDs), the proposed pacemaker for constrictions in these vessels, and an increase in the occurrence of action potentials. 3 Responses to histamine were inhibited by the H(1) receptor antagonist pyrilamine (0.2 micro M), but unaffected by NO synthase inhibition with N(G)-nitro L-arginine (L-NOARG, 100 micro M) and lysis of the endothelium. 4 In about 50% of the vessels, a decrease in constriction frequency, STD activity and a smooth muscle hyperpolarization were observed in response to dimaprit (10 micro M), suggesting the presence of H(2) receptors. These vessels had also a significantly lower basal contractile rate. Lymphatic vessel pumping was not affected by R-alpha-methylhistamine (10-50 micro M), ruling out a role for H(3) receptor stimulation in the histamine response. 5 The present results suggest a direct action of histamine on the lymphatic smooth muscle via stimulation of H(1) (and in some vessels H(2)) receptors. H(1) receptors enhance and H(2) receptors slow down lymphatic pumping, the dominant effect being an increased contractile activity. Correlation of these effects with histamine-induced changes in membrane potential and STD activity suggests the involvement of these electrical changes in the initiation of the contractile response.

Animals↗

PubMed1995

Blood and lymphatic vessel invasion as prognostic factors for patients with primary resected nonsmall cell carcinoma of the lung with intrapulmonary metastases.

BACKGROUND: The new classification of intrapulmonary metastases of lung cancer was proposed by the American Joint Committee on Cancer; however, the prognostic factors are heterogeneous and not yet fully clarified. In this study, the authors evaluated the prognostic factors for and the possible routes of intrapulmonary metastases. METHODS: The factors influencing the prognosis of primary resected nonsmall cell lung carcinomas with intrapulmonary metastasis in the resected specimens were evaluated according to the Cox proportional hazards model using a total of 66 nonsmall cell lung carcinomas. The possible routes of tumor spread via the blood or lymphatic vessels also were evaluated. RESULTS: The overall 5-year survival rate was 26.1%, and the statistical analysis of survival curves revealed a significant difference with regard to N classification (P = 0.042), site of intrapulmonary metastasis (P = 0.012), blood vessel invasion (P = 0.0046), and lymphatic vessel invasion (P = 0.0267); there were no significant differences in relation to age, sex, histology, differentiation, T classification, tumor size, stage, number of intrapulmonary metastases, or size of intrapulmonary metastasis. Multivariate analysis according to the Cox proportional hazards model identified a significant correlation between survival and blood vessel invasion (P = 0.044) and lymphatic vessel invasion (P = 0.042), suggesting independent prognostic significance. The correlation between site of intrapulmonary metastasis and the ratio of blood or lymphatic vessel invasion showed a significantly lower ratio of blood vessel invasion in cases with intrapulmonary metastases at sites central to the primary lesion or in different segment(s) compared with those in cases with intrapulmonary metastases at sites peripheral to the primary lesion or in ipsilateral different lobe(s), suggesting a possible lymphatic vessel route of tumor spread. CONCLUSION: Blood vessel and lymphatic vessel invasion are important clinical factors in evaluating prognosis and the route of tumor spread in primary resected nonsmall cell carcinoma with intrapulmonary metastasis.

Adult↗

PubMed2004

Inhibitory effects of the anesthetics propofol and sevoflurane on spontaneous lymphatic vessel activity in rats.

BACKGROUND: The effects of propofol and sevoflurane on lymphatic vessel activity are unknown. This study aimed to clarify the effects of these anesthetics on lymphatic vessel activity in rats by the use of a technique for mechanical removal of the endothelium. METHODS: The authors first examined the effects of propofol (8 mg/kg) and sevoflurane (2.0%) on in vivo lymphatic flow by injection of dye into the femoral regions of rats. In the in vitro study, the ends of the vessel segments of rat thoracic duct were connected to a syringe and stopcock, respectively. Spontaneous changes in diameter of each segment were monitored, and the extraluminal side of each segment was exposed to propofol (1 x 10(-6) approximately 3 x 10(-5) M) or sevoflurane (0.5 approximately 2.0%). Endothelial function was eliminated by perfusion of air into the lumen. RESULTS: In the dye uptake study, 80% of iliac lymphatic nodes were positively stained in a control group, whereas only 10% and 20% were positively stained in propofol and sevoflurane groups, respectively. In the in vitro study, both of the anesthetics significantly decreased the amplitude of spontaneous activity of lymphatic vessels with or without endothelial function. Sevoflurane inhibited the frequency of lymphatic vessel activity but propofol had no effect on it. When the endothelial function was eliminated, both anesthetics decreased the frequency of spontaneous activity of lymphatic vessels. CONCLUSIONS: Propofol and sevoflurane seem to have some different effects on endothelial function, which regulates the pacemaking of spontaneous contraction of lymphatic vessels.

Acetylcholine↗

PubMed2002

Lymphatic vessels in vascularized human corneas: immunohistochemical investigation using LYVE-1 and podoplanin.

PURPOSE: To determine whether lymphatic vessels exist in vascularized human corneas, by using immunohistochemistry with novel markers for lymphatic endothelium. METHODS: Human corneas exhibiting neovascularization secondary to keratitis, transplant rejection, trauma, and limbal insufficiency (n = 21) were assessed for lymphatic vessel content by conventional transmission electron microscopy and by immunostaining and immunoelectron microscopy with antibodies specific for the lymphatic endothelial markers, lymphatic vessel endothelial hyaluronan receptor (LYVE-1) and the 38-kDa integral membrane glycoprotein podoplanin. In addition, corneas were stained for the lymphangiogenic growth factor VEGF-C, and its receptor VEGFR3 by immunohistochemistry and in situ RNA hybridization, respectively. RESULTS: Thin-walled, erythrocyte-free vessels staining with lymphatic markers (LYVE-1 and podoplanin) were found to constitute 8% of all vessels, to be more common in the early course of neovascularization, to be always associated with blood vessels and stromal inflammatory cells, and to correlate significantly with the degree of corneal hemangiogenesis (r = 0.6; P = 0.005). VEGF-C, VEGFR3, podoplanin, and LYVE-1 colocalized on the endothelial lining of lymphatic vessels. With immunogold labeling, LYVE-1 and podoplanin antigen were found on endothelial cells lining vessels with ultrastructural features of lymph vessels. CONCLUSIONS: Immunohistochemistry with novel lymph-endothelium markers and ultrastructural analyses indicate the existence of lymphatic vessels in vascularized human corneas. Human corneal lymphangiogenesis appears to be correlated with the degree of corneal hemangiogenesis and may at least partially be mediated by VEGF-C and its receptor VEGFR3.

Adult↗

PubMed1995

The transendothelial passage in the absorbing peripheral lymphatic vessel of the rodent diaphragm.

The absorbing peripheral lymphatic vessels of rat (Wistar/Kyoto) and gerbil (Meriones unguiculatus) diaphragms were observed with SEM, TEM and three-dimensional models under normal conditions, after experimental hemorrhage and after abdominal injection of China ink and latex polystyrene particles. Superficial and deep lymphatic vessels were noted and their ultrastructural characteristics showed an endothelial wall lacking a continuous basal lamina. Moreover, "intraendothelial channels" which are dynamic, fundamental pathways for lumen migration into the lymphatic vessel for fluids, China ink and latex polystyrene particles, were also demonstrated. Concerning the transendothelial passage of the autologous erythrocytes after their migration through the stomata and submesothelium connective channel, it was observed that this passage occurs by means of a "transcellular pathway". This consists of a "migratory pore" independent from the intercellular junctions, which is formed by an active process following a probable immunological response or cellular interaction between the erythrocyte and the endothelial cell.

Animals↗

PubMed2003

Distribution of lymphatic vessels in normal and arthritic human synovial tissues.

OBJECTIVES: To investigate the distribution of lymphatic vessels in normal, rheumatoid arthritis (RA) and osteoarthritis (OA) synovium. METHODS: Synovial tissues from 5 normal controls, 14 patients with RA, and 16 patients with OA were studied. Lymphatic vessels were identified by immunohistochemistry using antibodies directed against the lymphatic endothelial hyaluronan receptor (LYVE-1) and recognised blood vessel endothelial markers (factor VIII, CD34, CD31). RESULTS: Lymphatic vessels were found in all zones of the normal, OA, and RA synovial membrane. Few lymphatic vessels were seen in the sublining zone in normal and OA synovium which did not show villous hypertrophy. However, in both RA synovium and OA synovium showing villous hypertrophy and a chronic inflammatory cell infiltrate, numerous lymphatic vessels were seen in all zones of the synovial membrane, including the sublining zone of the superficial subintima. CONCLUSIONS: Lymphatic vessels are present in normal and arthritic synovial tissues and are more numerous and prominent where there is oedema and an increase in inflammatory cells in the subintima, particularly in RA. This may reflect increased transport of hyaluronan and leucocyte trafficking in inflamed synovial tissues.

Arthritis, Rheumatoid↗

PubMed2006

Vascular endothelial growth factor-A mediates ultraviolet B-induced impairment of lymphatic vessel function.

UVB irradiation of the skin induces erythema, epidermal hyperplasia, vascular hyperpermeability, and edema formation. Previous studies have revealed that the cutaneous blood vasculature plays a critical role in the mediation of photodamage. In contrast, the role of lymphatic vessels, which play an essential role in the maintenance of tissue fluid balance, in the response to UVB irradiation has remained unknown. We report here that both acute and chronic UVB irradiation of murine skin results in prominent enlargement of lymphatic vessels. Surprisingly, these enlarged lymphatic vessels were functionally impaired and hyperpermeable, as detected by intravital lymphangiography. The expression levels of vascular endothelial growth factor (VEGF)-A but not of the known lymphangiogenesis factors VEGF-C or VEGF-D, were enhanced in UVB-irradiated epidermis. Targeted overexpression of VEGF-A in the epidermis of transgenic mice led to increased enlargement and leakage of lymphatic vessels after acute UVB irradiation, whereas systemic blockade of VEGF-A signaling largely prevented lymphatic vessel abnormalities and photodamage induced by UVB. Together, these findings identify lymphatic vessels as novel targets for UVB-induced cutaneous photodamage and suggest that VEGF-A mediates impairment of lymphatic vessel function, thereby contributing to the adverse effects of UVB irradiation on the skin.

Animals↗

PubMed1988

Intralobular lymphatic vessels and their relationship to blood vessels in the mouse thymus. Light- and electron-microscopic study.

The spatial distribution and fine structure of the lymphatic vessels within the thymic lobules of normal and hydrocortisone-injected mice were studied by light- and electron microscopy. The lymphatic vessels of the cortex and medulla of normal thymus are irregularly shaped spaces closely associated with branches of the intralobular artery and vein. The overall distribution of these vessels in the greatly involuted thymus of hydrocortisone-treated mice is essentially the same as in the normal thymus. The wall of the lymphatic vessels consists of only a layer of endothelial cells supported by underlying reticular cells. The luminal surface of the endothelial cell is smooth, but trabecular processes are often seen. There are three morphological types of intercellular contacts between contiguous cells, namely, end-to-end, overlapping and interdigitating. The lymphatic vessel has anchoring filaments and collagen fibrils, but a basal lamina is either absent, or if present, is discontinuous. This is in contrast to the continuous basal lamina of the venule. The perivascular space surrounding the postcapillary venule opens into a terminal lymphatic vessel at the cortico-medullary junction and in the medulla. Lymphocytes are seen penetrating the lymphatic endothelium, particularly in acutely involuted thymuses. These findings suggest that the intralobular lymphatic vessels may originate from the vacuities that surround the postcapillary venules, and the lymphatic system may function as a pathway for the migration of lymphocytes into or out of the lymphatic circulation.

Animals↗

PubMed2006

Absence of blood and lymphatic vessels in the developing human cornea.

PURPOSE: The normal human cornea is devoid of both blood and lymphatic vessels and actively maintains this avascularity (corneal angiogenic privilege). Whether and when corneal angiogenic privilege is achieved during development is unknown. METHODS: This study analyzed whether the cornea is primarily devoid of both blood and lymphatic vessels during intrauterine development or whether secondary regression of pre-existing vessels occurs before delivery. Indirect double immunohistochemistry was performed on 4-microm serial pupil-optic disc sections of paraffin-embedded human eyes stillborn at gestational ages of 17 to 41 weeks with antibodies against von Willebrand factor (vWF; factor VIII-associated antigen) as a panendothelial marker and with antibodies against lymphatic vessel endothelial hyaluronate receptor 1 (LYVE1) as a marker specific for lymphatic vascular endothelium. RESULTS: Human corneas were devoid of both vWF+++/LYVE-1(-) blood vessels and vWF+/LYVE-1+++ lymphatic vessels at all time-points analyzed. In contrast, there were numerous blood and lymphatic vessels detectable in the adjacent conjunctiva. CONCLUSION: The normal human cornea is primarily avascular and devoid of both blood and lymphatic vessels. Corneal angiogenic privilege is already achieved very early during fetal intrauterine development. This suggests early and strong expression of both antiangiogenic and antilymphangiogenic factors in the human cornea during development.

Blood Vessels↗

PubMed1989

Lymphatic vessel invasion is an independent prognostic factor for survival in colorectal cancer.

To assess whether lymphatic vessel invasion (LVI) is an independent prognostic factor in colorectal cancer, we retrospectively reviewed the records of 462 patients who underwent potentially curative surgery for carcinoma of the colon and rectosigmoid/rectum (rs/rectum) at the New England Deaconess Hospital from 1965-1978. Sixty-one patients were identified as having tumors with lymphatic vessel invasion (LVI+), and they were compared with the remaining group of 401 patients who had tumors without lymphatic vessel invasion (LVI-). The incidence of lymphatic vessel invasion was significantly increased in tumors with blood vessel invasion (24% vs. 5%, p = 0.000001). Patients with LVI+ tumors also had a significantly increased incidence of positive nodes (59% vs. 25%, p = 0.0004), the average number of positive nodes (4.8 vs. 2.2, p = 0.0003), and a lower 5-year survival rate (colon: 57% vs. 84%, p = 0.0001; rs/rectum: 38% vs. 71%, p = 0.004). There was a significant (p less than or equal to 0.05) increase in local (16% vs. 7%), abdominal (33% vs. 9%), and distant (13% vs. 4%) failure as a component of component of failure in patients with LVI+ colon cancer and a significant increase in abdominal (33% vs. 11%) and distant (13% vs. 8%) failure as a component of failure in patients with LVI+ rectosigmoid/rectal cancer. Proportional hazards analysis demonstrated that lymphatic vessel invasion was an independent prognostic factor for survival.

Adenocarcinoma↗

PubMed2007

Lymphatic vessel density at the site of deepest penetration as a predictor of lymph node metastasis in submucosal colorectal cancer.

PURPOSE: Lymph node metastasis is an important factor that influences curability after endoscopic treatment of submucosal colorectal cancer. This study was designed to determine the usefulness of identification of lymphatic vessels by immunohistochemistry in predicting lymph node metastasis of submucosal colorectal cancer. METHODS: Lymphatic involvement was assessed by hematoxylin and eosin staining and podoplanin immunostaining on samples resected from 268 patients with submucosal colorectal cancer. Lymphatic vessel density was estimated by two investigators by average count of three fields (x200) in the area of greatest number of podoplanin-positive capillaries at the site of deepest submucosal penetration. Relations with other clinicopathologic parameters also were investigated. RESULTS: Lesions with high lymphatic vessel density (> or =9 vessels per field) showed a significantly greater incidence of lymph node metastasis than did those with low lymphatic vessel density (<9 vessels per field; 23.3 vs. 8.4 percent). By multivariate analysis, lymphatic vessel density was determined to be an independent risk factor for lymph node metastasis of submucosal colorectal cancer (P = 0.0044). Lymphatic vessel density also correlated with tumor budding and the degree of inflammation at the invasive front. CONCLUSIONS: Identification of lymphatic vessels by podoplanin immunostaining provides objective and accurate evaluation of lymphatic involvement. Lymphatic vessel density at the site of deepest penetration is a useful predictor of lymph node metastasis of submucosal colorectal cancer.

Colorectal Neoplasms↗

PubMed1990

Organization of the lymphatic vessels and their relationships to blood vessels in rabbit Peyer's patches.

The three-dimensional organization of the lymphatic vessels and their relationship to blood vessels in rabbit Peyer's patches were demonstrated by scanning electron microscopy (SEM) of corrosion casts and of tissues. The interconnected central lacteals in the villi overlying the interfollicular area were connected with the lymphatic plexus in the area. There were many blind-ending lymphatic vessels in the upper part of the interfollicular area. These lymphatics gradually fused and formed perifollicular lymphatic sinuses which surrounded the lateral surfaces and bottoms of the follicles. There were no lymphatic vessels within the dome and the follicle. The perifollicular lymphatic network surrounded the capillary network of the follicle. Between the perifollicular lymphatic networks in the interfollicular area were many high endothelial venules (HEVs) which collected the capillaries in the dome and the follicle. The voluminous perifollicular lymphatic sinuses seemed to have a great potential capacity as both reservoirs and as drainage routes for fluid and lymphocytes. The close association of HEVs with the perifollicular lymphatic vessels seemed to facilitate the prompt drainage of fluid and macromolecules leaking out of HEVs during lymphocyte migration into the lymphatics. That the HEVs are downstream of the capillaries in both the dome and the follicle suggests that substances such as cytokines may be involved in the induction of the post capillary venules into HEVs.

Animals↗

PubMedDate not supplied

Lymphatic vessels and lymphangiogenesis in female cancer: mechanisms, clinical impact and possible implications for anti-lymphangiogenic therapies (Review).

Lymphatic vessels play a crucial role in a variety of human cancers, since invasion of lymphatic vessels by tumor cells and subsequent development of lymph node metastases significantly influences prognosis of cancer patients and therefore represent an integral part of tumor staging. Recent evidence on the important influence of lymphangiogenetic growth factors on intralymphatic cancer growth and metastasis raises hopes that lymphatic vessels and factors inducing their growth could serve as an additional target for tumor therapy. Nevertheless, in contrast to blood vessel angiogenesis, the mechanisms of new lymphatic vessel formation in human cancers, i.e. lymphangiogenesis, are still relatively unclear. In addition, only little data exist so far on the quantification and impact of this lymphangiogenesis, evident by lymphatic microvessel density (LMVD), on the prognosis of cancer patients. With expectation of possible anti-lymphangiogenic therapies, this review focuses on the mechanisms of lymphangiogenesis in general, and especially on the role of lymphatic vessels in gynecological and breast cancer, which are the so far most detailed investigated malignancies with regard to lymphangiogenesis.

Endothelial Growth Factors↗

PubMedDate not supplied

Lymphatic vessels of healthy and inflamed gingiva.

Lymphatic vessels were traced in healthy and early inflamed gingivae of various nonhuman primates. Lymphatic capillaries and primary collecting vessels originated in the connective tissue papillae and stroma near or adjacent to the attachment epithelium. They emptied into thin-walled irregular-shaped collecting vessels that drained into the periodontal ligament. In early inflammation, all the lymphatic vessels of luminal caliber were distended within and/or surrounding the inflammatory infiltrate.

Animals↗