Key result
Prostaglandins E1 and ω-homo-E1 inhibited ADP-induced platelet aggregation and transient thrombocytopenia in vivo, with PGE1 increasing the LD50 of ADP in young rats.
Why the study?
Do Prostaglandins E1 and ω-homo-E1 inhibit ADP-induced platelet aggregation in vivo in young rats?
Do Prostaglandins E1 and ω-homo-E1 inhibit ADP-induced platelet aggregation in vivo in young rats?
Answers are grounded in this paper and cite their sources.
Prostaglandins E1 and ω-homo-E1 inhibit ADP-induced platelet aggregation in vivo, preventing fatal platelet thrombi in rats.
Summary Prostaglandins E1 and ω-homo-E1 which were shown previously to inhibit adenosine diphosphate (ADP)-induced platelet aggregation in vitro have now been found to inhibit this process also in vivo. Both prostaglandins inhibit transient thrombocytopenia induced by intravenous injection of ADP; PGE1 increases also the LD 50 of ADP when injected in high amounts into young rats. In both cases platelet aggregation in vivo is the primary cause of the phenomena observed. The symptoms observed on overdosing ADP by intravenous injection are unconsciousness within 10-20 sec after completion of the injection immediately followed by respiratory arrest and eventual death of the animal, generally within 10 min. It seems that blocking of the supply of blood to the brain by platelet thrombi, which on histological examination were found to occlude blood vessels in different organs, is the most important causative factor of the symptoms observed.
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J Kloeze (1970) studied ADP-induced platelet aggregation. Prostaglandins E1 and ω-homo-E1 was evaluated on Transient thrombocytopenia and LD50 of ADP. Prostaglandins E1 and ω-homo-E1 inhibited ADP-induced platelet aggregation and transient thrombocytopenia in vivo, with PGE1 increasing the LD50 of ADP in young rats.
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