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Homocysteinemia increased significantly after a methionine load of 50 mg/kg in patients with peripheral artery occlusive disease but this load was insufficient to increase circulating endothelial cell count as a marker of endothelial damage. Only after an increased load of 100 mg/kg methionine circulating endothelial cells also increased markedly confirming the results of a previous experimental study. These data indicate a threshold concentration of homocysteine in blood necessary to induce endothelial lesions.

The author presents an account of the main contemporary findings on the functional importance of heparan sulphate (HS), which is an important part of the endothelial glycocalyx. Based on the ability to form complexes with proteins, HS interferes in particular with antithrombotic properties of the endothelium and modulates in a significant way the proliferative activity of the endothelium and other cells of the vascular wall. The author mentions its pathogenetic role, possibilities of its diagnostic use and therapeutic perspectives in the area of vascular diseases.

Changes of blood vessel endothelium in psoriasis have not been fully documented in the literature. The aim of our study was to ascertain whether in cases of such involvement an increase of endothelaemia could be identified. The counts of circulating endothelial cells were significantly increased in psoriatics compared with healthy individuals and patients with atopic eczema. The explanation of this observation may be based on the endothelial cell replacement stimulation in psoriasis.

A humoral transfer of a factor inducing a decrease of circulating endothelial cells (CEC) released during venostasis was demonstrated in rats. The possibility to block its activity by an in-vitro addition of protamine suggests its identity with an endogenous heparan sulfate possessing an inhibitory effect on endothelial turnover. This was supported by an analogous effect of intravenously administered heparan sulfate-related agent.

Administration of putrescine, a polyamine, to rats leads to endothelial injury manifesting itself by an increased number of endothelial cells circulating in blood. Moreover, putrescine affects the metabolism of the arterial wall itself, primarily by increasing the activity of phosphomonoesterases I and II and by decreasing the activities of Krebs cycle enzymes, both of which are phenomena that can be regarded as "preatherogenic" changes 5, 6, 8, 11 preceding the onset of pathological processes in the arterial wall. Putrescine significantly decreases aortic ATPase (adenylpyrophosphatase) both in the acute and chronic phases of experiment. Ultrastructural changes after 16 weeks of putrescine administration manifested themselves in increased proliferation and smooth muscle cell injury eosinophil inflitration into the adventitia. The findings support the hypothesis that high levels of PA in homocysteinemic patients and those on chronic dialysis are a common denominator accelerating atherosgenesis in these subjects.

In connection with the increasing importance of the endothelium in understanding the pathogenesis of vascular diseases, new types of mediators originating in the endothelium are described, such as EDRF and endothelin. The method of endothelial cell cultivation has contributed to their detection. Besides such analytical methods, a more global in vivo aspect of endothelial function is dealt with by the method of counting circulating endothelial cell carcasses in blood applicable also clinically. The increase of endothelaemia goes hand in hand with both the tendency to thrombosis and increased permeability. Similarly, the main atherosclerotic risk factors, smoking, hypertension and hypercholesterolaemia could be effective by producing an endothelial perturbation as indicated by increased endothelaemia.

A method for indicating latent endothelial lesion based on circulating endothelial cell count after methionine challenge was used in a group of hypertensives and in healthy controls. A significantly increased cell count was found in hypertensives.

An attempt was made to show that a special methodology based on functional in vivo aspects (induction of increased enothelemia by suitable challenges) may help to obtain an integrated and potentially useful new look at both the pathogenesis and therapy of thrombosis and atherosclerosis.

Chronic administration of methionine to rats induced endothelial lesion manifested by increased endothelaemia and metabolic changes indicative of pathological processes involving the vessel wall. These changes did not spontaneously return to values observed in control animals. Long-term administration of antiatherosclerotic drugs Pyridinolcarbamate and Phtalazinole II normalized metabolic disorder in the aortic wall and reduced endothelaemia to normal values.