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Journal ArticleDOI

The effect of prostaglandin E1 on platelet function in vitro and in vivo.

TLDR
It is concluded that the effect of PGE1 on haemostasis involves inhibition of the release of ADP from platelets exposed to collagen and thrombin, and inhibition ofADP‐induced aggregation.
Abstract
Summary Low concentrations of prostaglandin E1 (PGE1) inhibit ADP-induced aggregation in pig and rabbit citrated platelet-rich plasma and in suspensions of washed platelets. Higher concentrations also inhibit the initial change in shape induced by ADP and the release of platelet ATP, ADP and serotonin caused by stimuli such as collagen, thrombin, antigen-antibody complexes and gamma-globulin-coated polystyrene particles. PGE1 is not taken up by platelets and its effects can be removed by resuspending platelets in fresh medium. Immediately following an intra-arterial injection, ADP-induced platelet aggregation is suppressed, but after 5 min the response returns to normal. PGE1 inhibits haemostasis in rabbits when given as a continuous infusion. It is concluded that the effect of PGE1 on haemostasis involves inhibition of the release of ADP from platelets exposed to collagen and thrombin, and inhibition of ADP-induced aggregation.

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Book ChapterDOI

The role of Prostaglandin E1 in patients with critical leg ischemia

TL;DR: Since 1987, PGE1 (Prostavasin) has been used predominantly intravenously, and the first convincing results in patients treated via this route are published; the compound is registered in Japan, Germany, Italy, Austria and some other countries for the treatment of ischemic rest pain and trophic ulcerations.
Journal ArticleDOI

Rabbit lung macrophages stimulate platelets in vitro as observed by density-gradient centrifugation and transmission electron microscopy.

TL;DR: Addition of platelet antagonists showed that the shift in platelet density and the rosetting upon contact with macrophages are dependent on divalent cations.
Journal ArticleDOI

Effect of adenosine 5′-diphosphate and shape change on 5-hydroxytryptamine uptake by human blood platelets

TL;DR: The rate of uptake of 5-HT in human platelets measured in citrated platelet-rich plasma (PRP) is unaffected by shape change induced either by low temperature or low adenosine 5′-diphosphate (ADP, 0.5 μM) concentrations, and the reversible blocking action of ADP on 5- HT uptake described for rats does not appear to occur in man.
Journal Article

Effect of infusion of prostaglandin E1 on the aggregation of blood platelets in man.

TL;DR: The effects of intravenous (i.v.) infusion of prostaglandin E1 (PGE1) on thrombocyte aggregation in humans were studied in 3 healthy male volunteers and no discernable effects was found.
Book ChapterDOI

Effect of Agents which Modify Platelet Aggregation and/or Coagulation on Experimental Platelet Embolism and Intravascular Coagulation

TL;DR: It is obvious, and already well known, that platelet aggregation and coagulation are concurrent and both play a vital role in the pathogenesis of most ischemic strokes in atheromatous patients.
References
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Journal ArticleDOI

Prostaglandins: Their Disappearance from and Release into the Circulation

TL;DR: The liver and lungs provide an efficient protective mechanism to remove almost all the prostaglandin before it reaches the arterial circulation.
Journal ArticleDOI

Adenosine diphosphate-induced platelet aggregation in suspensions of washed rabbit platelets.

TL;DR: On comparison with rabbit platelets prepared from blood taken into EDTA, the only differences observed were the much greater sensitivity to ADP and a higher calcium content; platelet morphology, nucleotide levels, and conversions of 14C‐ATP and 14C-ADP at the platelet membrane were similar.
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