PubMed Health⌕ Search

Biomedical subjects

E Glusa

Publications and source records attributed to E Glusa.

14 recordsLinked to original sources
PubMed1979

[Inhibition of blood platelet function].

Blood platelets play a decisive role in haemostasis and thrombosis. Besides the known approaches for preventing thrombosis by inhibition of the plasmatic coagulation, it seems promising to prevent thrombus formation, particularly in the arterial vasculature, by pharmacological control of platelet functions. Drugs with antiaggregating effects are described from the clinico-pharmacological point of view. Non-steroidal antiphlogistics - especially acetylsalicylic acid - several vasodilators, alpha- and beta-adrenergic receptor blockers, as well as some others have been used therapeutically. To test these drugs for the prophylaxis of thrombosis, long-term prospective clinical trials are necessary.

Adrenergic alpha-Antagonists↗
PubMed1979

Studies on the inhibition of adrenaline-induced aggregation of blood platelets.

alpha-Adrenoceptors of platelets seem to differ from those of other cell types. The inhibitory effect of alpha-adrenoceptor-blocking agents on adrenaline-induced aggregation of human platelets does not parallel that on adrenaline-induced contraction of rabbit aortic strips. The most potent inhibitors of adrenaline-induced platelet aggregation are the dihydrogenated ergot alkaloids of the peptide type. Among the other ergoline derivatives testes, only lisuride has a stronger inhibitory effect than those of natural ergot alkaloids.

Adrenergic alpha-Antagonists↗
PubMed1979

[Effect of ergoline derivatives on platelet and blood vessels].

The influence of dihydrogenated ergot alkaloids on vessels and blood platelets was studied in vitro and in vivo. At low concentrations they cause contraction of isolated vein strips via a stimulation of alpha-adrenoceptors, at higher concentrations they antagonize the action of noradrenaline on arteries and veins and inhibit the adrenaline-induced platelet aggregation in vitro. In volunteers, intravenous and subcutaneous administration of dihydroergotamine (Dihytamin) caused a decrease in blood volume of the capacitance vessels and inhibition of the adrenaline-potentiated platelet aggregation "ex vivo". The selective venoconstrictor and antiaggregating effects of dihydroergotamine are utilized in the postoperative prophylaxis of thrombosis.

Adrenergic alpha-Antagonists↗
PubMed1979

[Effect of ASS on platelet function in experimental DIC].

In thrombin-induced DIC, acetylsalicylic acid (ASA) prevents the strong initial fall in platelet count and the obturation of the microvasculature of the lung with platelet aggregates. During the DIC reaction increasing inhibition of aggregability of circulating platelets against collagen and ADP is observed. Furthermore, ASA prevents the increase in the plasma haemoglobin level caused by DIC.

Animals↗
PubMed1979

[Interactions of platelet inhibitors].

Combination effects of inhibitors of platelet function with different mechanisms of action such as adenosine, acetylsalicylic acid, papaverine, dipyridamole, and sodium nitroprusside were studied in vitro by means of ADP- and collagen-induced aggregation of human blood platelets. In case of ADP-induced aggregation, potentiation of the inhibitory effect was observed only with the combination adenosine-papaverine, whereas in case of collagen-induced aggregation the inhibitory effect was potentiated at various inhibitor combinations.

Adenosine↗
PubMed1978

[Possibilities of prevention and therapy of arteriosclerosis by influencing hemostatic functions].

Thrombotic processes play a role not only as a sequel of arteriosclerosis, but also for its pathogenesis. Under this aspect a pharmacological regulation of the course of the reaction of thrombpcytes, the blood coagulation and the fibrinolysis gets significance. The prevention of the formation of fibrin by well-known anticoagulants, such as coumarines and heparin, seems little suited for a prophylaxis of arteriosclerosis. By a pharmacological regulation of the reaction of the blood platelets which are decisive for the initial phase of the formation of thrombi new possibilities for an intervention into the pathomechanisms of arteriosclerosis are the result. Her also realizations concerning the prostaglandin metabolism of the blood platelets and of the wall of vessels can be evaluated. The activation of fibrinolysis by means of the hitherto introduced fibrinolytics, such as streptokinase and urokinase, is used above all for the treatment of acute thrombi. In the sense of a prevention of arteriosclerosis the activation of the endogenic fibrinolysis with the help of indirect fibrinolytics, which effect a liberation of the activators of fibrinolysis localised in the wall of the vessels, is a hopful way.

Anticoagulants↗
PubMed1978

Influence of pentacyanoferrate complexes on platelet aggregation.

To elucidate the structural constituents of sodium nitroprusside responsible for antiaggregating effects, comparative studies were done with pentacyanoferrates possessing ligands other than nitric oxid. Among the pentacyanoferrates tested, also the nitro and thionitro compounds possess considerable antiaggregating effects. The ammine and aquo compounds are nearly ineffective. These results support the assumption that the nitrosyl cation or its secondary product, nitrous acid, is responsible for the inhibition of aggregation.

Ferricyanides↗
PubMed1978

[Pharmacological effect of pentacyanonitrosylferrate and similar complex compounds].

Comparative studies were performed on the spasmolytic and hypotensive effects of pentacyanoferrates with different ligands (NO, NO2, NOS, NH3, H2O) and of hexacyanoferrates and other nitrosyl compounds. Besides sodium nitroprusside, the nitro and thionitro complexes in equimolar doses were found to cause hypotension and relaxation of the aortic strip of rabbits contracted by adrenaline and spasmolytic effects on the contracted guinea pig ileum. The liberated nitrosyl cation or its secondary product, nitrous acid, is thought to be responsible for the pharmacodynamic effects of these complex compounds. This is in agreement with the fact that also other nitrosyl compounds (nitrosyl perchlorate, nitrosyl-bis(dimethylglyoximato)cobaltIII) and free undissociated nitrous acid produce transient spasmolytic effects. Pentacyanoaquoferrate and hexacyanoferrateIII exert, presumably because of the oxydation of sulfhydryl groups, spasmolytic effects in vitro. Accordingly, their effects are prevented in the presence of sulfhydryl compounds such as glutathion or dithioerythrit.

Animals↗