Increased production of prostacyclin after injury to the microvasculature in uraemic patients

Slazus W. (1992)


The original publication is available at


A recently described method to evaluate the primary haemostatic mechanism under in vivo conditions was utilised to investigate thromboxane A2 (TXA2) and prostacyclin (PC12) 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. PC12 - produced by microvascular endothelial cells after a standardised injury - was, however, 59% higher inpatients than controls (P < 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.

Please refer to this item in SUNScholar by using the following persistent URL:
This item appears in the following collections: