Vascular endothelial damage

Hemolytic-uremic syndrome presents as a Coombsnegative microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency, and the outcome is often fatal. The underlying pathology is thought to be vascular endothelial damage. It occurs 4-7 months after the start of chemotherapy. Blood transfusion can cause clinical deterioration in those affected (9). Histology of... 

Thomas T, Thomas G, McLendon C, Sutton T, Mullan M. 1996. Beta-amyloid-mediated vasoactivity and vascular endothelial damage. Nature 380 168-71... 

Pulmonary vascular endothelial damage with fluid extravasation and necrosis of surrounding tissue... 

Vascular endothelial damage and hemorrhagic necrosis of adrenal medulla, anterior pituitary, right atrium retroperitoneal gelatinous edema... 

On the other hand, there is growing evidence for the role of the nitric oxide radical ( NO) in vascular endothelial damage. It is speculated that ( NO) scavenging activity may contribute to the therapeutic effects of the flavonoids. On the basis of this hypothesis,recently the ( NO) scavenging capacity of certain flavonoids, as hydroxyethylrutosides, has been investigated by Van Acker et al. [188],... 

This syndrome is characterized by a reddening of the palms and the soles of the feet. It is thought to be due to vascular endothelial damage caused by the drug. 

Belzer, F.O., Hoffman, R, Huang, J. and Downs, G. (1972). Endothelial damage in perfused dc kidney and cold sensitivity of vascular Na-K-ATPase. Cryobiology 9, 457-460. 

Growth factor facilitates vascular endothelial cell, vascular smooth muscle cell, and fibroblast multiplication and growth, leading to repair of damaged blood vessels. 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

Protection of vascular endothelial cells from oxygen free radical damages Enhancement of SOD, catalase and peroxidase in the cytosol of kidney Protection of pulmonary endothelium against free radicals in rabbits Protection of lipid peroxidation in liver and cardiac muscle in rats Inhibition of lipid peroxidation of rat liver and brain microsomes Inhibition of lipid peroxidation in serum and liver in rats Protective effect of ginsenosides on reperfusion injuries... 

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