[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.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000648:ultrastructure; D002046:Bupranolol / Q000031:analogs & derivatives / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D008854:Microscopy, Electron; D010974:Platelet Aggregation / Q000187:drug effects*; D011412:Propanolamines / Q000494:pharmacology*; D013237:Stereoisomerism
D011412:Propanolamines; D000244:Adenosine Diphosphate; D002046:Bupranolol; D001241:Aspirin
Zur Hemmung der Thrombozytenaggregation durch Bupranolol. Eine aggregometrische und elektronenmikroskopische In-vitro-Studie.