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Biomedical subjects

J Hladovec

Publications and source records attributed to J Hladovec.

At least 19 recordsLinked to original sources
PubMed1992

Heparan sulfate as a venostatic endothelial stabilizing factor.

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.

Animals↗
PubMed1992

[Lipoperoxides and atherosclerosis].

The theory of the pathogenetic role of lipoperoxides in atherosclerosis and thrombosis is very topical at present. It unifies the theory on the role of free oxygen radicals with the theory of damage of the vascular wall and with the theory of impaired lipid metabolism. It makes possible also a new interpretation of known risk factors. It is also based on the most recent results of molecular biology (role of monocytes-macrophages).

Animals↗
PubMed1991

The effect of polyamines on the endothelium and vascular wall metabolism in the rat.

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.

Animals↗
PubMed1991

Antithrombotic effects of heparin and related agents.

Native heparin was very effective in models of arterial and venous thrombosis as well as in a model demonstrating the effect on endothelial stability in rats. The effect on venous thrombosis was particularly prominent. The activities of LMW-heparin were about the same in all three models, the absolute effective dose against arterial thrombosis being much lower than with native heparin. A heparan sulfate-related preparation (suleparoide) was much less effective in both thrombosis models, especially in the venous one, while the activity was most specifically directed to the maintenance of endothelial stability.

Animals↗
PubMed1990

Antithrombotic activity of an unsaturated fatty acid preparation.

An unsaturated fatty acid preparation from fish oil, "Epavit", completely prevented arterial thrombosis induced in the rat aorta by a combined stenosis, extensive endothelial perturbation and i.v. serotonin, at an optimum dose of 0.1 ml/200 g orally. A partial effect lasted more than 18 hours. After repeated administrations the acute completely inhibitory effect was decreased but the partial and chronic one remained unchanged. Aspirin (ASA) showed no synergic activity. Venous thrombosis (one-sided ligature of the caval vein combined with extensive endothelial perturbation) was inhibited to a similar degree as arterial thrombosis. Epavit also prevented the destabilizing effect of i.v. citrate on the endothelial lining.

Animals↗
PubMed1979

Is the antithrombotic activity of "antiplatelet" drugs based on protection of endothelium?

In only five "antiplatelet" agents has the antithrombotic activity been confirmed both clinically and experimentally. These include acetylsalicylic acid, dipyridamole, clofibrate, hydroxychloroquine and sulfinpyrazone. Whereas only acetylsalicylic acid has a demonstrable effect on platelet aggregation in doses usually applied, the effects of all remaining drugs are more easily explained by their influence on the vessel wall. This assumption is supported by the finding that all five drugs possess a stabilizing effect on endothelium in doses corresponding closely to the clinical dose range. The method based on counting detached endothelial cells in blood after a standard stimulus was used to demonstrate this effect.

Animals↗
PubMed1979

Experimental homocystinemia, endothelial lesions and thrombosis.

A single intravenous injection of homocystine led to an increase in the number of circulating endothelial cells in the blood of rats. We observed also increased permeability of the lung capillaries, platelet sequestration and activation of the venostatic thrombosis. Endothelial injury is probably the key mechanism of thrombotic and atherosclerotic complications in homocystinuria, an inborn error of the amino acid metabolism.

Animals↗
PubMed1979

The influence of calcium antagonists on endothelium.

Calcium antagonists possess, similarly to endothelotropic (vasotropic) drugs, a stabilizing effect on endothelium against the disrupting influence of citrate in rats. This was demonstrated with the new method for counting of circulating endothelial cells. The effect is dose related and the effective experimental dosages corresponded closely to the clinical dose range. The common link between both drug groups is probably the mediating effect of ionic calcium.

Animals↗
PubMed1978

Endothelial injury by nicotine and its prevention.

Nicotine administered i.v. or p.o. in doses above 0.0125 mg/kg to the rat caused a highly significant increase in circulating anuclear carcasses of endothelial cells estimated by an original method. This effect of nicotine was completely prevented by a prior oral administration of the flavonoids hydroxyethylrutosides (HR) or Mono-7-HR.

Animals↗
PubMed1978

Circulating endothelial cells in acute myocardial infarction and angina pectoris.

The authors have counted circulating anuclear carcasses of endothelial cells by a new method in 105 patients with acute myocardial infarction and angina pectoris. In infarction cases as well as in severe angina a significant increase of endothelaemia was observed in duration of several days. No increase was observed in milder angina cases (type I--II).

Angina Pectoris↗
PubMed1978

Circulating endothelial cells as a sign of vessel wall lesions.

A new method of endothelaemia estimation was used to investigate the production of vessel wall lesions by various drugs in rats. Increased endothelaemia was observed after endotoxin, activation of the blood contract system, hyaluronidase, streptokinase, anoxia and vasoactive drugs.

Animals↗
PubMed1977

Vasotropic drugs--a survey based on a unifying concept of their mechanism of action.

A group of vasotropic drugs was surveyed using a new assay method based on the inhibition of endothelaemia increases after a standard vascular lesion in rats. The new test is considerably more sensitive than all previous ones. It provides a common link between all tested vasotropic drugs and points also to their common mechanism of action. All of them have a protective effect on endotherlium based, in some of them at least, on the preservation of the consistency of endothelial cement. The effect is probably mediated by their influence on calcium availability.

Animals↗
PubMed1977

Differentiation of in vitro and in vivo effects of a flavonoid on endothelial cell counts.

Parenterally administered flavonoids decrease endothelaemia in rats as determined by a new method in two ways: in vivo and in vitro. The in vitro effect caused by flavonoids present in blood might interfere with the cell counting and can be eliminated by neutralization of flavonoids with cobaltous ions. The resulting endothelial counts represent the "true" in vivo effect. Using this method it has been shown that the in vitro interference did not modify significantly the previously demonstrated marked effect of a flavonoid (mono-7-hydroxyethylrutoside) on increased endothelial counts after provocation with citrate.

Animals↗
PubMed1977

Antithrombotic effects of some flavonoids alone and combined with acetylsalicylic acid.

In the rat, a selection of two experimental models of "prethrombotic states", one of venostatic thrombosis and one of arterial thrombosis was used to compare the antithrombotic of three flavonoid preparations: O,-(beta-hydroxyethyl)-rutosides (HR), an association of trihydroxyethylrutoside and coumarin (troxerutin) and 7-mono-hydroxyethylrutoside (7-Mono-HR), as well as acetylsalicylic acid (ASA). The flavonoids were very effective "protectors" on the prethrombotic models, but only ASA was active on the model of arterial thrombosis. No compound showed a clear protection on the venostatic model if direct activation by kaolin was used. However, if an indirect activation by vessel wall stimulation was used, 7-Mono-HR possessed a marked protective effect. The most favourable results were obtained with an association of 7-Mono-HR and ASA, which could be considered for investigation in clinical thrombosis prophylaxis.

Animals↗
PubMed1976

Decrease of endothelaemia during immunosuppression.

The counts of circulating endothelial cells estimated by a new quantitative method were significantly decreased in a group of patients after renal transplantation. Subsequent animal studies have shown that such a decrease may be attained by the administration of immunosuppressive drugs. The explanation of this observation may be based on the suppression of a normal endothelial cell replacement.

Animals↗