6-ketoprostaglandin-f1-alpha and Cadmium-Poisoning

Here, using our original technique for measuring of thrombogenesis on the surface of rabbit aorta endothelium superfused with whole blood, we demonstrate that the thrombogenic property of endothelium is potentiated in the course of 3 months cadmium intoxication. The loss of endothelial thromboresistance is accompanied by suppressed generation of endogenous prostacyclin, leukopenia, increased platelet aggregability and by the presence of quasi-atherosclerotic, focal proliferative, glassy-protein lesions formed in aortic endothelium. We hypothesize that the final loss of vessel thromboresistance with all sequence of events that accompany cadmium intoxication, may result from the cadmium-induced inhibition of the generation of endothelial prostacyclin. However, the exact mechanism by which cadmium intoxication may affect the generation of prostacyclin and, then, functioning of blood platelets and vascular endothelium requires further investigations.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Cell Count; Blood Pressure; Cadmium; Cadmium Poisoning; Endothelium, Vascular; Immunity, Innate; Male; Platelet Aggregation; Rabbits; Radioimmunoassay; Thrombosis