Increased production of prostacyclin after injury to the microvasculature in uraemic patients.
A recently described method to evaluate the primary haemostatic mechanism under in vivo conditions was utilised to investigate thromboxane A2 (TXA2) and prostacyclin (PGI2) production by platelets and vascular endothelial cells, respectively, in patients with severe chronic renal failure. Unlike some previous studies, a decrease in TXA2 production by uraemic platelets could not be demonstrated. PGI2--produced by microvascular endothelial cells after a standardised injury--was, however, 59% higher in patients than controls (P less than 0.05). An increased local level of this potent platelet inhibitory eicosanoid could play an important role in the bleeding tendency exhibited in chronic renal failure.
Slazus
W
W
Department of Haematological Pathology, University of Stellenbosch.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis / Q000097:blood; D001760:Bleeding Time; D001792:Blood Platelets / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism*; D008297:Male; D008833:Microcirculation / Q000378:metabolism*; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000097:blood; D014511:Uremia / Q000150:complications
D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol