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Biomedical subjects

F Markwardt

Publications and source records attributed to F Markwardt.

At least 217 records · Page 12Linked to original sources
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↗
PubMed1978

Inhibition of adrenaline-potentiated thrombin-induced reaction of human blood platelets by dihydroergotoxine.

The potentiating effect of adrenaline on thrombin-induced aggregation and release reaction of human blood platelets has been studied in vitro. Both reactions are inhibited by low doses of dihydroergotoxine. The inhibition of aggregation is of competitive type. The adrenaline-potentiated thrombin-induced platelet aggregation is inhibited also after intravenous injection of dihydroergotoxine. The pathophysiological implications of these findings are discussed.

Blood Platelets↗
PubMed1978

[Influence of mediators on plasminogen activator release].

The influence of substances known as low molecular weight mediators such as biogenic amines, peptides and prostaglandins on the plasminogen activator release was studied in the isolated perfused pig ear. Among the substances tested, histamine and the plasma kinins bradykinin and kallidin were found to possess a dose-dependent activator-releasing effect, which in case of histamine can be suppressed by an antihistamine (promethazine). Serotonin and the prostaglandins at concentrations up to 10(-5)M possess no significant activator-releasing effect. Compared with the biogenic peptides angiotensin, oxytocin, vasopressin, and eledoisin, only the latter was found to release plasminogen activator. Studies on the influence of the substances tested on the capillary permeability showed that enhanced permeability is caused only by those mediators which cause also increased activator release.

Animals↗
PubMed1977

Heparin-induced release of plasminogen activator.

The influence of heparin and heparinoids on the release of plasminogen activator was studied in the isolated perfused pig ear. Heparin enhances the release of the tissue activator of fibrinolysis in a dose-dependent manner within the range of 0.05-1.0 IU/ml perfusion fluid. The release is also caused by sulfated polyanions at concentration of 10 microgram/ml.

Animals↗
PubMed1977

[Animal experimental studies on the thrombolytic effect of ocrase].

The thrombolytic effect of "ocrase", a protease isolated from Aspergillus ochraceus, was investigated in animal experiments. To prevent general hyperproteolysis a protease dose was used which was was neutralized by the inhibitors in the blood of the animals. Experimentally produced deposition and clotting thrombi in peripheral venous or arterial vessels of mice, rats, dwarf pigs and dogs were lysed by regional and systemic administration, and the therapeutic result was estimated by vital microscopy, rheography or angiography. Coronary thrombosis induced in dwarf pigs was treated semilocally with ocrase, and the therapeutic result was followed by ECG and angiography.

Animals↗