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Fibrin split product D-dimer (DD) is most probably involved in the development of vascular disorders. At 1.5 uM concentration DD inhibited the incorporation of D-[1-3H]glucosamine hydrochloride and [2-14C]acetate • Na into pericellular heparan sulphate (HS) of rabbit coronary endothelial cells without affecting other groups of glycosaminoglycans (GAGs). At the same time, DD reduced HS ability to bind antithrombin (AT) and suppressed NO production. The effect of DD on pericellular GAGs was similar to that of Nω-methyl-L-arginine, the competitive inhibitor of endo­thelial NO synthase (eNOS). L-Ascorbic acid, eNOS activator, increased the level of en­dogenous NO in the DD-treated cells, and restored HS accumulation and antithrombin binding. It is suggested that DD influence on endothelial HS may be me­diated by NO production. Another effect of DD, namely, stimulation of plasminogen activator inhibitor-1 (PAI-1) secretion did not depend on the NO level. The decreased HS content, reduced anticoagulant properties of HS, and increased PAI-1 secretion disorganized the endothelial matrix, and promoted fibrin formation and vascular damage. This points to DD as an important factor in the development of vascular disorders.
The aim of the study was to determine the relationship between estrogen and the development of peliosis hepatis. The experiment was conducted on female Wistar rats. Oestradiolum benzoicum was administered i.m. for 8 weeks in different doses. On the basis of the obtained data the authors claim that estrogen can be responsible for the development of vascular disorders described as peliosis hepatis. Furthermore, there is a relationship between the intensification of observed changes and the dose of the injected estrogen. An increased awareness of peliosis hepatis may become an important symptom for a pathologist, especially in patients at risk.
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Endothelial-mediated regulation of cerebral microcirculation

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Vascular endothelial cells are important not only for maintaining homeostasis, but also in pathogenesis of vascular disorders. Cerebral capillary and microvascular endothelial cells play an active role in maintaining cerebral blood flow, microvascular tone and blood brain barrier functions. Factors produced and released by endothelial cells, other brain cells and circulating blood cells participate in these regulatory functions. In particular, endothelin-1 (ET-1) and nitric oxide (NO) are known to contribute to the functional vascular changes under pathological conditions (e.g., hypertension, arteriosclerosis, and stroke). This report describes the involvement of endothelial cell mediators in the post-ischemic hypoperfusion induced by brain ischemia and in vitro endothelial responses (Ca2+ mobilization and cytoskeletal rearrangements) to ET-1 and its interactions with NO or 2-AG. The capacity of NO and endocannabinoids to counteract ET-1-induced cerebral capillary and microvascular endothelial responses indicates that they may actively participate in EC function and implicates them in physiological and pathophysiological conditions.
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