Prevention of Endothelial Damage by Special Precautions during Implantation

2015 ◽  
pp. 54-58
Author(s):  
J. Draeger
Keyword(s):  
Endothelial Damage

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

Circulating Thrombomodulin as a Clue of Endothelial Damage in Behçet’s Disease

1996 ◽  
Vol 75 (06) ◽  
pp. 974-975 ◽  
Author(s):  
İbrahim C Haznedaroğlu ◽  
Oktay Özdemir ◽  
Osman Özcebe ◽  
Semra V Dündar ◽  
Şerafettin Kirazli
Keyword(s):  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Behçet's Disease ◽  
Endothelial Damage ◽  
Behcet's Disease

An Electron Microscopic Study of Platelet Thrombus Formation in the Rabbit with Particular Regard to 5-Hydroxytryptamine Release

1967 ◽  
Vol 18 (03/04) ◽  
pp. 592-604 ◽  
Author(s):  
H. R Baumgartner ◽  
J. P Tranzer ◽  
A Studer
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vessel Wall ◽  
Thrombus Formation ◽  
Endothelial Damage ◽  
Electron Microscopic ◽  
Rabbit Ear ◽  
Basement Lamina ◽  
Platelet Thrombus

SummaryElectron microscopic and histologic examination of rabbit ear vein segments 4 and 30 min after slight endothelial damage have yielded the following findings :1. Platelets do not adhere to damaged endothelial cells.2. If the vessel wall is denuded of the whole endothelial cell, platelets adhere to the intimai basement lamina as do endothelial cells.3. The distance between adherent platelets as well as endothelial cells and intimai basement lamina measures 10 to 20 mµ, whereas the distance between aggregated platelets is 30 to 60 mµ.4. 5-hydroxytryptamine (5-HT) is released from platelets during viscous metamorphosis at least in part as 5-HT organelles.It should be noted that the presence of collagen fibers is not necessary for platelet thrombus formation in vivo.

Impaired Fibrinolysis in Sickle Cell Disease

1970 ◽  
Vol 24 (01/02) ◽  
pp. 010-016 ◽  
Author(s):  
D Green ◽  
H. C Kwaan ◽  
G Ruiz
Keyword(s):  
Sickle Cell Disease ◽  
Factor Viii ◽  
Plasminogen Activator ◽  
Sickle Cell ◽  
Fibrinolytic Activity ◽  
Endothelial Damage ◽  
Cell Disease ◽  
Clotting Factors ◽  
Platelet Counts

SummaryCoagulation studies were performed in 52 patients with sickle cell disease during asymptomatic periods and during episodes of crisis and infection. Platelet counts averaged 473,000, 469,000, and 461,000 per mm3 in these 3 groups, and factor VIII concentrations were elevated in all. Fibrinogen was increased to the same extent in both sickle cell and non-sickle cell patients with infection. Fibrinolytic activity, as measured by euglobulin lysis times and zones of lysis on fibrin plates, was markedly reduced during periods of infection in sickle cell patients but not in non-sickle patients. Impairment of fibrinolysis in most patients was not on the basis of overutilization or consumption, since no decrease in the levels of clotting factors or plasminogen was observed. It was suggested that generalized intravascular sickling in these patients may have caused widespread endothelial damage, resulting in decreased production of plasminogen activator.In addition, several sickle cell patients with infection were found to possess elevated levels of an inhibitor directed against urokinase.

Protective Effect of Vitamin E on Immune Triggered, Granulocyte Mediated Endothelial Injury

1984 ◽  
Vol 51 (01) ◽  
pp. 089-092 ◽  
Author(s):  
M A Boogaerts ◽  
J Van de Broeck ◽  
H Deckmyn ◽  
C Roelant ◽  
J Vermylen ◽  
...  
Keyword(s):  
Vitamin E ◽  
Protective Effect ◽  
Umbilical Vein ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Mediated Effects ◽  
Anti Oxidant ◽  
Endothelial Cell Cultures ◽  
Vitro Model

SummaryThe effect of alfa-tocopherol on the cell-cell interactions at the vessel wall were studied, using an in vitro model of human umbilical vein endothelial cell cultures (HUEC). Immune triggered granulocytes (PMN) will adhere to and damage HUEC and platelets enhance this PMN mediated endothelial injury. When HUEC are cultured in the presence of vitamin E, 51Cr-leakage induced by complement stimulated PMN is significantly decreased and the enhanced cytotoxicity by platelets is completely abolished (p <0.001).The inhibition of PMN induced endothelial injury is directly correlated to a diminished adherence of PMN to vitamin E- cultured HUEC (p <0.001), which may be mediated by an increase of both basal and stimulated endogenous prostacyclin (PGI2) from alfa-tocopherol-treated HUEC (p <0.025). The vitamin E-effect is abolished by incubation of HUEC with the irreversible cyclo-oxygenase inhibitor, acetylsalicylic acid, but the addition of exogenous PGI2 could not reproduce the vitamin E-mediated effects.We conclude that vitamin E exerts a protective effect on immune triggered endothelial damage, partly by increasing the endogenous anti-oxidant potential, partly by modulating intrinsic endothelial prostaglandin production. The failure to reproduce vitamin E-protection by exogenously added PGI2 may suggest additional, not yet elucidated vitamin E-effects on endothelial metabolism.

Potential role of an endothelium-specific growth factor, hepatocyte growth factor, on endothelial damage in diabetes

Diabetes ◽  
1997 ◽  
Vol 46 (1) ◽  
pp. 138-142 ◽  
Author(s):  
R. Morishita ◽  
S. Nakamura ◽  
Y. Nakamura ◽  
M. Aoki ◽  
A. Moriguchi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Potential Role ◽  
Specific Growth ◽  
Endothelial Damage ◽  
Specific Growth Factor ◽  
Hepatocyte Growth
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