Comparison of umbilical vein models for measurement of relative prostacyclin and thromboxane production

Abstract

There is growing evidence that blood vessels generate TXA 2 in addition to PGI 2. We examined effluents from continously perfused human umbilical vein and supernatants from umbilical vein rings for TXB 2 and 6-keto-PGF 1α measurements (stable metabolites of TXA 2 and PGI 2, respectively). TXB 2 and 6-keto-PGF 1α were identified in all samples. 6-keto-PGF 1α to TXB 2 ratio was higher in intact vein effluents than in the venous ring supernatants (112:1 and 28:1, respectively, P<0.01). Arachidonate stimulation increased 6-keto-PGF 1α and TXB 2 levels similarly in the intact vein effluent. In contrast, stimulation of the venous rings resulted in a relatively larger increase in TXB 2 than in 6-keto-PGF 1α. This caused 6-keto-PGF 1α to TXB 2 ratio to decline (p<0.01). The identity of TXB 2 was confirmed in several different ways. These data suggest that 1) human umbilical veins produce TXA 2 in addition to PGI 2, 2) TXA 2 release is more by venous rings than by the intact vein probably reflecting contribution from non-endothelial layers, and 3) arachidonate stimulation causes relatively greater release of TXA 2 than of PGI 2 from the venous rings, whereas release of PGI 2 and TXA 2 is similar from the intact vein.