Impairment of Platelet Thromboxane A<sub>2</sub> Generation and of the Platelet Release Reaction in Two Patients with Congenital Deficiency of Platelet Cyclo‐oxygenase

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<jats:p>Two cases of thrombocytopathia with congenital deficiency of platelet cyclo‐oxygenase were investigated. The platelet release reaction was impaired. There was a marked decrease of aggregation with collagen and with adrenalin and a total absence of aggregation with sodium arachidonate. The platelet response to labile aggregation stimulating substance (LASS, mostly thromboxane A<jats:sub>2</jats:sub>) was normal. There was no biosynthesis of prostaglandin cyclic endoperoxides or of thromboxane A<jats:sub>2</jats:sub> from arachidonic acid. Basal levels of platelet PGE<jats:sub>1</jats:sub> were lowered although plasma levels were normal. Thrombin decreased the cyclic AMP content of patients' platelets and also that of control platelets pretreated with aspirin. The patients' platelets showed no ultrastructural difference when compared with control platelets, except for a slight decrease of granule volume, but, in contrast to control platelets, thrombin (0.02 U/ml) did not provoke contraction of the patients' platelets.</jats:p>

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