path(MESH:"Vascular System Injuries")
By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury 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
Heme may be implicated and contribute to the development of (i) bp(MESH: PubMed:26875449
An increase in plasma cell-free Hb and vascular dysfunction also has been shown after transfusion of autologous RBCs with long storage duration to healthy human subjects.19,20,37 PubMed:27308950
Hemolysis and the transfusion of banked blood or Hb-based therapeutics can result in varying quantities of circulating acellular Hb which can induce life threatening radical generating reactions in patients with a compromised vascular system [60]. PubMed:24486321
Free hemoglobin (Hb) triggered vascular damage occurs in many hemolytic diseases, such as sickle cell disease, with an unmet need for specific therapeutic interventions. PubMed:26475040
Depending on the scale, rate, and site of hemolysis, the primary adverse effects triggered by free Hb are vascular dysfunction, oxidative tissue damage, and altered inflammatory response [1], PubMed:26475040
Several studies in animals have supported the idea that infusion of free Hb, stored RBC supernatant (preservation solution + plasma), and Hb-containing microvesicles causes vasoconstriction, vascular dysfunction, and vascular injury.12,16–18 PubMed:27308950
Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082
Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082
Furthermore superoxide can react with Hb to produce hydrogen peroxide (H2O2), a well defined prooxidative molecule that causes vascular injury (1). 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
By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury model. PubMed:19276082
Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082
Furthermore superoxide can react with Hb to produce hydrogen peroxide (H2O2), a well defined prooxidative molecule that causes vascular injury (1). PubMed:19276082
Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082
Hemolysis and the transfusion of banked blood or Hb-based therapeutics can result in varying quantities of circulating acellular Hb which can induce life threatening radical generating reactions in patients with a compromised vascular system [60]. PubMed:24486321
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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.