Compounds > 6-ketoprostaglandin-f1-alpha

6-ketoprostaglandin-f1-alpha and Hemorrhagic-Disorders

6-ketoprostaglandin-f1-alpha has been researched along with Hemorrhagic-Disorders* in 1 studies

Other Studies

1 other study(ies) available for 6-ketoprostaglandin-f1-alpha and Hemorrhagic-Disorders

Article	Year
Vascular thromboxane formation in hemostasis mechanism: correlation between bleeding time and vascular TXB2 in a patient with congenital platelet cyclo-oxygenase deficiency. International journal of hematology, 1996, Volume: 63, Issue:4 We encountered a patient with congenital platelet cyclo-oxygenase deficiency with normal ability to synthesize vascular prostaglandin I2 (PGI2) and thromboxane A2 (TXA2). The patient's peripheral blood monocytes did not show cyclo-oxygenase (COX) activity, but cultured bone marrow fibroblasts showed COX activity. To determine the mechanism of primary hemostasis in this patient, we examined the effect of oral administration of aspirin (1 g) on bleeding time and thromboxane B2 (TXB2), 6-keto prostaglandin F1 alpha (6-keto-PGF1 alpha) production in the blood emerging from the incision in this patient. The bleeding time was markedly prolonged by the administration of aspirin, and this prolongation was associated with the inhibition of TXB2 in the effluent blood, which seemed to be derived from the vessel wall. These findings suggest that vascular TXA2 production plays an important role in the maintenance of hemostasis. Topics: 6-Ketoprostaglandin F1 alpha; Administration, Oral; Adult; Arteries; Aspirin; Bleeding Time; Blood Platelets; Bone Marrow; Cyclooxygenase Inhibitors; Endothelium, Vascular; Epoprostenol; Female; Fibroblasts; Hemorrhagic Disorders; Humans; Isoenzymes; Monocytes; Platelet Aggregation Inhibitors; Prostaglandin-Endoperoxide Synthases; Thromboxane B2; Uterus	1996

Article

Year

Vascular thromboxane formation in hemostasis mechanism: correlation between bleeding time and vascular TXB2 in a patient with congenital platelet cyclo-oxygenase deficiency.

International journal of hematology, 1996, Volume: 63, Issue:4

We encountered a patient with congenital platelet cyclo-oxygenase deficiency with normal ability to synthesize vascular prostaglandin I2 (PGI2) and thromboxane A2 (TXA2). The patient's peripheral blood monocytes did not show cyclo-oxygenase (COX) activity, but cultured bone marrow fibroblasts showed COX activity. To determine the mechanism of primary hemostasis in this patient, we examined the effect of oral administration of aspirin (1 g) on bleeding time and thromboxane B2 (TXB2), 6-keto prostaglandin F1 alpha (6-keto-PGF1 alpha) production in the blood emerging from the incision in this patient. The bleeding time was markedly prolonged by the administration of aspirin, and this prolongation was associated with the inhibition of TXB2 in the effluent blood, which seemed to be derived from the vessel wall. These findings suggest that vascular TXA2 production plays an important role in the maintenance of hemostasis.

Topics: 6-Ketoprostaglandin F1 alpha; Administration, Oral; Adult; Arteries; Aspirin; Bleeding Time; Blood Platelets; Bone Marrow; Cyclooxygenase Inhibitors; Endothelium, Vascular; Epoprostenol; Female; Fibroblasts; Hemorrhagic Disorders; Humans; Isoenzymes; Monocytes; Platelet Aggregation Inhibitors; Prostaglandin-Endoperoxide Synthases; Thromboxane B2; Uterus

1996