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Results for “vascular endothelium”

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At least 19 recordsLinked to original sources

PubMed1979

Seeding arterial prostheses with vascular endothelium. The nature of the lining.

Arterial prostheses seeded with autogenous vascular endothelium demonstrate a well-organized, cellular, inner lining. To determine the nature of the lining cells, six animals underwent replacement of the infrarenal aorta with Dacron prostheses. During the preparation of three such grafts, endothelium was scraped from the saphenous vein with a steel wool pledget, suspended in chilled Sack's solution, and mixed with blood used to preclot the graft. This suspension was omitted from the three control grafts. After six weeks, the grafts were removed, rinsed and examined. Fluorescent Factor VIII related antigen (F VIII-RA) strongly stained the lining cells. Silver nitrate Haütchen and electron microscopy preparations revealed a lining pattern characteristic of vascular endothelium. Endothelial cell-specific Weibel-Palade bodies were identified in the lining cell cytoplasm. Masson's trichrome staining revealed a relatively collagen-poor connective tissue within the seeded fabric. Transmission electron microscopy disclosed vascular smooth muscle cells between the seeded graft fabric and the lining cells. Vasa vasorum, arising from the outer capsule, penetrated the fabric to supply the inner capsules of the seeded grafts. It is concluded that the cells lining seeded canine arterial prostheses are true vascular endothelium supported by vascular smooth muscle cells, that the lining contains minimal connective tissue, and that vasa vasorum develop. Unseeded control grafts lacked these features.

Animals↗

PubMed1979

[Vascular endothelium (author's transl)].

Studies during recent years have shown the importance of the vascular endothelium in several physiological and pathological circumstances. The culture of endothelial cells has permitted the direct study of endothelial functions. The endothelium is a selective barrier between blood and tissues: the molecules cross it, according to their size, either through the intercellular junctions or through the cells by pinocytotic vesicles. The permeability is modulated by vasomotor agents and modified during endothelial regeneration, especially for the lipids. The endothelium plays a prominent part in the maintenance of the blood flow through its nonthrombogenic properties. It metabolizes circulating thrombogenic substances (arachidonic acid, adenosine diphosphate) and produces potent antiaggregating agents (prostacyclin and adenosine). It may also release a plasminogen activator promoting thrombolysis. The endothelial cells contribute to the formation of the basement membrane by synthesizing collagen and fibronectin, which are involved in platelet adhesion and aggregation to exposed subendothelium. On the other hand, the endothelium has a modulating influence on the local blood flow by producing vasoconstrictors (angiotensin II and III) and vasodilating agents (adenosine and prostacyclin). It is not necessary to elucidate the coordination of these functions and their relationship to the endothelial disorders in vascular diseases.

Actins↗

PubMed1976

alpha2-Macroglobulin on human vascular endothelium.

alpha2-Macroglobulin (alpha2M) has been identified on the luminal surface of endothelial cells in sections of normal human arteries, veins, and lymphatics by the indirect immunofluorescent technique. The specificity of the immunofluorescent reaction was confirmed by immunoabsorption studies. Prior absorption of the anti-alpha2M antiserum by purified alpha2M at equivalence completely inhibited endothelial surface as well as hepatic parenchymal cell staining. Endothelial cells in blood vessels were not stained when sections were treated with rabbit antisera toward alpha1-antitrypsin, antithrombin III, IgG, IgA, IgM, C3, or fibrinogen. The location of alpha2M at the surface of the vessel wall suggests that this protease inhibitor may protect the vascular endothelium from potentially injurious intravascular proteases.

Blood Vessels↗

PubMed1976

Transformation of cultured human vascular endothelium by SV40 DNA.

Primary cultures of human umbilical vein endothelial cells (HEC) developed extensive cytopathic changes and necrosis after high multiplicity infection with wild-type SV40 virus. Using the calcium co-precipitation technique, stable transformation was obtained with purified preparations of intact circular SV40 DNA and restriction endonuclease-derived linear DNA fragments containing the entire early gene region. Smooth muscle cells, isolated from the same blood vessels, showed neither cytopathic effects nor transformation after similar treatment with SV40 virus or DNA. The HEC cultures transformed by SV40 (SVHEC) expressed SV40-specific T (tumor) and Tr (transplantation) antigens, but not V (viral capsid) antigen. No evidence of infectious virus production was found upon co-cultivation with the CV-1 line of monkey kidney cells. Transformation resulted in markedly increased growth potential, loss of anchorage dependence and topoinhibition of growth, and a reduced serum requirement. Prolonged subcultivation was accompanied by chromosomal abnormalities and eventual "crisis". Transformed cells did not exhibit endothelial-specific organelles (Weibel-Palade bodies) or factor VIII antigen, but angiotensin-converting enzyme occasionally was detectable in SVHEC cultures. SV40-transformed human vascular endothelium, a nonfibroblast diploid cell type, may be useful in studies of oncogenesis and control of the differentiated state.

Antigens↗

PubMed1979

Increased interaction of vascular endothelium and leucocytes after administration of antiplatelet serum: role in the developing vascular defect.

Antiplatelet serum (APS) induced an increase in the stickiness of white cells which manifests itself in the increase in number of granulocytes rolling along or sticking to the venous endothelium. Lidocaine treatment prevented the increased stickiness of white cells and, at the same time, the microvascular haemorrhage developing after APS. It can be assumed that increased stickiness of white cells after APS may contribute to endothelial damage.

Animals↗

PubMed1978

The care of vascular endothelium in pediatric surgery.

The influence of manipulating blood vessels by clamping, drying, stretching and surgical anastomotic technique on the subsequent integrity of blood vessel endothelium has been studied in the dog. Thrombogenesis at the vessel surface was found in all specimens where loss of endothelium had exposed subendothelial tissues. Whether thrombotic occlusion of the vessel followed depended upon several local factors including the amount of surface area damaged and volume of blood flow in the vessel. All modes of vessel manipulation studied led to significant endothelial damage. To prevent this damage in the clinical setting all possible methods to avoid the exposure of subendothelial tissues should be used. Endothelial integrity is the cornerstone to success in handling blood vessels and avoiding thrombogenesis. This study suggests that clamping of blood vessels should always be done with a minimum of force, only preventing blood flow, and not crushing the vessel wall. Endothelial surfaces should never be allowed to become dry. Stretching should be avoided as it can lead to thrombosis within intact blood vessels when the endothelium is disrupted. Suture anastomotic techniques should be used which minimize endothelial trauma and thus avoid subendothelial tissue reactions which in turn may jeopardize long-term patency and growth at anastomotic sites. In pediatric cases where growth is anticipated interrupted suture technique should be used. This study suggests that many techniques currently used in vascular surgery may be compromising to short and long-term blood vessel patency.

Animals↗

PubMed1978

Relationship between lymphocyte emigration and vascular endothelium in chronic inflammation.

Small blood vessels within areas of chronic inflammation which contain large numbers of lymphocytes develop unusually thick walls. Combined histological and electron microscope study shows that the thickening is due to hypertrophy of endothelial cells which come to resemble the endothelium of post-capillary venules in lymphoid tissue. Vessels of this type have been found in experimental granulomas induced by injection of Freund's adjuvant or killed tubercle bacilli and in human biopsy material from cases of rheumatoid arthritis and Hashimoto's disease of the thyroid. Comparison with the developing Peyer's patch in young rats shows that the unusual vessels in granulomas are very similar in endothelial cell size, pattern of distribution, extent of lymphocyte migration and degree of carbon leakage to post-capillary venules of the immature Peyer's patch. Study of the time at which lymphocytes appear in large numbers within the granuloma or developing Peyer's patch and the time at which thickened vessels are first seen suggest tha the endothelial changes are a consequence and not a cause of lymphocyte emigration. The stimulus to endothelial hyperthrophy appears to be massive sustained migration of lymphocytes, but the functional significance of this change in vascular structure is not clear.

Animals↗

PubMed1976

Permeability of pulmonary vascular endothelium.

Three aspects of transendothelial exchange in the lungs are considered: stretching of interendothelial junctions of pulmonary microvessels by increase in pulmonary capillary pressures; selective stretching of interendothelial junctions of bronchial venules in response to histamine, bradykinin and endotoxin; active transport of peptides across the body of the endothelial cell after enzymic action at or near the luminal surface of the endothelial cell. Stretching of interendothelial junctions between the cells lining the pulmonary capillaries was demonstrated using a variety of macromolecular tracers under controlled haemodynamic conditions. Selective leakage of bronchial venules, the systemic venules of the lungs, was shown using colloidal carbon as a tracer. Transendothelial transport of peptides across the pulmonary capillary lining involved the use of electron microscopic autoradiography after intravenous administration of radioactively-labelled lipoproteins. Different mechanisms appear to provide routes of entry into the perivascular interstitial spaces of the lungs.

Animals↗

PubMed1979