prostaglandin-d2 and Blood-Platelet-Disorders

In 2 male patients (35 and 38 years) presenting with myocardial infarction an abnormal conversion of exogenous 14C-arachidonic acid by the patients' platelets, incubated in vitro, was observed. Neither patient's platelets showed evidence of a lipoxygenase pathway. Platelet thromboxane formation from exogenous and endogenous substrate was high, while the platelet aggregation responses were normal. A myeloproliferative syndrome was excluded by bone marrow puncture. Similar defects have only been described so far in patients with myeloproliferative syndrome. This defect may be causative for the onset of clinical thrombotic events. It is speculative whether in vivo therapy with r-IFN alpha 1c might be able to eradicate the pathological platelet clone.

Topics: Adult; Arachidonic Acids; Blood Platelet Disorders; Blood Platelets; Chromatography, Thin Layer; Dinoprostone; Humans; Lipoxygenase; Male; Myocardial Infarction; Platelet Aggregation; Prostaglandin D2; Thromboxanes

Topics: Adenocarcinoma; Aged; Aged, 80 and over; Blood Platelet Disorders; Blood Platelets; Female; Humans; Myeloproliferative Disorders; Pancreatic Neoplasms; Platelet Aggregation; Prostaglandin D2; Prostaglandins D

The mechanism as well as some characteristics of haematin-induced human platelet aggregation were investigated. Haematin-induced platelet aggregation required the presence of devalent cations; Mg2+, and to a lesser extent, Co2+, were just as effective as Ca2+ in supporting the aggregation. Mono- and trivalent cations were ineffective. Verapamil inhibited the aggregation. The aggregation was accompanied by thromboxane formation which could be abolished by aspirin. The release of adenine nucleotides was only slightly inhibited by aspirin. The rate of aggregation and the ultrastructure of the aggregated platelets were comparable between control and aspirin-treated samples. It is concluded therefore that haematin-induced aggregation is not dependent on platelet prosta-glandin synthesis. Haematin induced binding of fibrinogen to platelets, and failed to aggregate thrombasthenic platelets. These findings indicate that haematin may induce platelet aggregation by promoting influx of divalent cations in association with increased fibrinogen binding and release of adenine nucleotides.

Topics: Adenosine Triphosphate; Apyrase; Blood Platelet Disorders; Blood Platelets; Cations, Divalent; Child; Epoprostenol; Female; Fibrinogen; Heme; Hemin; Heparin; Humans; Microscopy, Electron; Platelet Aggregation; Prostaglandin D2; Prostaglandins D; Prostaglandins, Synthetic; Thromboxanes; Verapamil