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Summary. It is known that in most cases of transmural acute myocardial infarction a platelet clot originates within a coronary artery. In acute myocardial infarction patients increased levels of the plasma catecholamines adrenaline and noradrenaline as well as the platelet release proteins platelet factor 4 and fl-thromboglobulin have been reported. In this study, significantly higher values were found of platelet factor 4 ( P < 0.0001) and flthromboglobulin (P < 0.002) in 17 acute myocardial infarction patients as compared to 17 control patients (on intensive care due to non-cardiac disorders), while the plasma levels of adrenaline and noradrenaline were not different. Positive correlations were obtained between the two catecholamines and the platelet products in the control group and between adrenaline and both platelet factor 4 ( r = 0 . 7 1 5 , P < 0 . 0 1 ) and fl-thromboglobulin (r = 0.547, P < 0.05) in the acute myocardial infarction patients. The data suggest that a stimulation of the platelets by adrenaline may facilitate in vitro activation during sampling in patients with high catecholamine load. On the other hand, a "preactivation" of the platelets by an increase of adrenaline might be of significance for thrombus formation in acute myocardial infarction.

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Purified melanosomes isolated from subcutaneously growing Harding-Passey melanomas of NMRI-mice were labeled either in vitro with [14C] tyrosine or [14C]DOPA in the melanin portion, or in vivo in the melanin and protein portion following i. p. injection of [14C] tyrosine. Treatment of monolayer cultures of Harding-Passey melanoma cells (HPM-73 line) with such labeled melanosomes resulted in rapid uptake of label during the first 4 h which leveled off thereafter. A portion of the “incorporated” label could be removed by a 15 min chase with unlabeled melanosomes.Uptake of labeled melanosomes by HPM-73 cells was followed by increased cellular melaniza­tion which was not only due to melanin derived from incorporated melanosomes but primarily to newly formed melanin. Tyrosinase activity was elevated in melanosome-treated cells. Tyrosinase activity of control cells was significantly reduced following a 24 h exposure to actinomycin D or cycloheximide. On the other side, the same inhibitor treatment of melanosome-pretreated cells resulted in less inhibition of tyrosinase activity.The present findings suggest “melanophagic” properties of cultured melanoma cells resulting in enhanced melanogenesis after phagocytotic uptake of functionally active exogenous melanosomes.

Serum removal from the media of serial monolayer cultures of the Harding-Passey melanoma during an incubation period of 3 days resulted in an exponentially declining DNA synthesis rate (measured by the incorporation of [14C] thymidine) and in an inhibition of cell proliferation. Pro­tein synthesis, as measured by the incorporation of radioactive leucine, was less affected than DNA synthesis. Incubation in serum-free culture medium resulted in significant rises of tyrosinase ac­tivity and cellular melanin content. Addition of dibutyryl adenosine 3′ :5′ monophosphate (Bu2cAMP, 5×10-4ᴍ) and theophylline (5×10-4 ᴍ) to serum-free cultures caused a further striking increase of tyrosinase activity and melanin formation, while treatment of serum containing cultures with Bu2cAMP and theophylline showed only a slight rise in melanogenesis. It is sug­gested that these stimulatory effects are mediated by an increased intracellular cAMP level, since a correlation between the degree of melanogenesis and cellular cAMP content was indicated. Treat­ment of serum-free or serum-containing cultures with the phosphodiesterase inhibitor theophylline (5×10-4 - 1×10-3 ᴍ) alone revealed only a slight enhancement (about 20%) of melanogenesis. Because augmentation of melanogenesis by serum-free medium alone or together with Bu2cAMP and theophylline was prevented by cycloheximide (or actinomycin D), de novo protein synthesis seems to be required for these stimulatory effects.