[On the inhibition of thrombocyte aggregation by bupranolol / Aggregometric and electron microscopic study in vitro (author's transl)].

The ADP-induced primary aggregation of human thrombocytes in vitro was inhibited by 1.5X10(-4) mol/l (+/-)bupranolol. At this concentration a strong desaggregation was obtained. The stereoisomers of bupranolol did not differ in effectiveness. Fractional addition was just as effective as a single dose. Not beta-receptor blocking but a membrane stabilizing effect is, therefore, the probable mechanism -- as in the case of propranolol. The less lipophilic metabolites hydroxybupranolol and carboxybupranolol were one-fourth and one-fifth as effective, respectively, as bupranolol. 5X10(-4) mol/l ASA (final concentration) showed the same inhibition of primary aggregation as did 1.5X10(-4) mol/l bupranolol but elicited less desaggregation. Doubling this dose of ASA resulted in a weaker inhibition than the subsequent addition of the aforementioned doses of bupranolol and ASA or vice versa, while this combination, in turn, inhibited less than a double dose of bupranolol. 1.5X10(-4) mol/l bupranolol inhibited the formation of pseudopodia by thrombocytes not stimulated with ADP. At 3X10(-4) mol/l this inhibition was drastic but no morphological damage was seen.