a(CHEBI:"iron trichloride")
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
FeCl3 treatment resulted in a dose- (Fig. 3) and timedependent (data not shown) increase inRBClipid peroxidation, which correlated closely with hemolysis (Fig. 2B). PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
Analysis of Hb release from ex vivo vessel chamber experiments revealed a significant (p 0.05; n 4) increase in Hb levels following FeCl3 treatment of isolated aorta in the presence of flowing blood (157 45 g/ml), whereas FeCl3 pretreatment of vessels prior to blood perfusion caused no hemolysis (Fig. 2A). PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
To investigate the direct effects of FeCl3 on aortic endothelium, FeCl3 was perfused through isolated aorta independently of flowing blood. Strikingly no endothelial denudation or collagen exposure was evident following prolonged exposure to FeCl3 (6%) (Fig. 1C). PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
In contrast, selectively removing RBCs prevented endothelial denudation and collagen exposure, resulting in a relatively mild perturbation of endothelial function similar to that observed with FeCl3 alone (data not shown). PubMed:19276082
High concentrations of FeCl3 induce profound injury to the vasculature, leading to endothelial denudation, and collagen and tissue factor exposure, leading to the rapid formation of vaso-occlusive thrombi. PubMed:19276082
As demonstrated in Fig. 1, topically exposing aorta in vivo (Fig. 1A) or ex vivo (Fig. 1B) to 6% FeCl3 resulted in major vascular injury as evidenced by endothelial denudation, collagen exposure, and the subsequent formation of arterial thrombi (Fig. 1D and supplemental Video 1). PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
High concentrations of FeCl3 induce profound injury to the vasculature, leading to endothelial denudation, and collagen and tissue factor exposure, leading to the rapid formation of vaso-occlusive thrombi. PubMed:19276082
As demonstrated in Fig. 1, topically exposing aorta in vivo (Fig. 1A) or ex vivo (Fig. 1B) to 6% FeCl3 resulted in major vascular injury as evidenced by endothelial denudation, collagen exposure, and the subsequent formation of arterial thrombi (Fig. 1D and supplemental Video 1). PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
To investigate the direct effects of FeCl3 on aortic endothelium, FeCl3 was perfused through isolated aorta independently of flowing blood. Strikingly no endothelial denudation or collagen exposure was evident following prolonged exposure to FeCl3 (6%) (Fig. 1C). PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
In contrast, selectively removing RBCs prevented endothelial denudation and collagen exposure, resulting in a relatively mild perturbation of endothelial function similar to that observed with FeCl3 alone (data not shown). PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
Subsequent perfusion of anticoagulated whole blood through FeCl3-pretreated vessels was associated with an increase in leukocyte and platelet adhesion to the vessel wall (Fig. 1E and supplemental Video 2); however, relative to untreated aorta (Fig. 1F and supplemental Video 3) and treatment in the presence of flowing blood (Fig. 1D and supplemental Video 1), thrombus formation was not observed. PubMed:19276082
Analysis of Hb release from ex vivo vessel chamber experiments revealed a significant (p 0.05; n 4) increase in Hb levels following FeCl3 treatment of isolated aorta in the presence of flowing blood (157 45 g/ml), whereas FeCl3 pretreatment of vessels prior to blood perfusion caused no hemolysis (Fig. 2A). PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082
FeCl3 treatment resulted in a dose- (Fig. 3) and timedependent (data not shown) increase inRBClipid peroxidation, which correlated closely with hemolysis (Fig. 2B). PubMed:19276082
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.