Influence of Intravenously Administered Acetylsalicylic Acid on Platelet Functions

1975 ◽  
Vol 4 (1) ◽  
pp. 12-22
Author(s):  
H. Vinazzer ◽  
J. Pütter ◽  
D. Loew
1996 ◽  
Vol 49 (5) ◽  
pp. 351-354
Author(s):  
D. Pallapies ◽  
A. Muhs ◽  
L. Bertram ◽  
G. Rohleder ◽  
P. Nagyiv�nyi ◽  
...  

1996 ◽  
Vol 49 (5) ◽  
pp. 351-354 ◽  
Author(s):  
D. Pallapies ◽  
A. Muhs ◽  
L. Bertram ◽  
G. Rohleder ◽  
P. Nagyiványi ◽  
...  

1977 ◽  
Author(s):  
J. Hladovec

On the basis of a new test for counting circulating endothelial cells in blood, a group of drugs was redefined which prevent endothelial desquamation after a standard intravenous injection of citrate into rats. The group comprised practically all drugs designated as venotonics or vitamin P-active agents, including some haemostatics, analgesic-antipyretics (acetylsalicylic acid) and some antiatherosclerotics (pyridinolcarbamate, Clofibrate). A marked activity was observed also with several calcium-antagonists (nifedipine, prenylamine, chromonar, dipyridamole and verapamil). Many endothelotropic drugs are simultaneously effective in blocking platelet functions. The suggested common mechanism of action is the influence on the consistency of the cellular surface coat (endothelia cement).


1976 ◽  
Vol 36 (02) ◽  
pp. 376-387 ◽  
Author(s):  
Teruhiko Umetsu ◽  
Kazuko Sanai ◽  
Tadakatsu Kato

SummaryThe effects of bupranolol, a new β-blocker, on platelet functions were investigated in vitro in rabbits and humans as compared with propranolol, a well-known β-blocker. At first, the effect of adrenaline on ADP-induced rabbit platelet aggregation was studied because adrenaline alone induces little or no aggregation of rabbit platelets. Enhancement of ADP-induced rabbit platelet aggregation by adrenaline was confirmed, as previously reported by Sinakos and Caen (1967). In addition the degree of the enhancement was proved to be markedly affected by the concentration of ADP and to increase with decreasing concentration of ADP, although the maximum aggregation (percent) was decreased.Bupranolol and propranolol inhibited the (adrenaline-ADP-)induced aggregation of rabbit platelets, bupranolol being approximately 2.4–3.2 times as effective as propranolol. Bupranolol stimulated the disaggregation of platelet aggregates induced by a combination of adrenaline and ADP, but propranolol did not. Platelet adhesion in rabbit was also inhibited by the β-blockers and bupranolol was more active than propranolol. With human platelets, aggregation induced by adrenaline was inhibited by bupranolol about 2.8–3.3 times as effectively as propranolol.From these findings. We would suggest that bupranolol might be useful for prevention or treatment of thrombosis.


1980 ◽  
Vol 44 (03) ◽  
pp. 143-145 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
J Gormsen

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.


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