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Inhibition of vascular epoprostenol (prostacyclin, PGI2) production in vitro by plasma from healthy subjects and patients with severe renal impairment.

1982; Wiley; Volume: 14; Issue: 3 Linguagem: Inglês

10.1111/j.1365-2125.1982.tb01994.x

1365-2125

Ritter Jm, Orchard Ma, Lewis Pj,

Inflammatory mediators and NSAID effects

OHS1 The production of 6-oxo-prostaglandin Flia (6-oxo-PGFia) and epoprostenol (prostacyclin, PGI2) by fresh rat aortic rings were measured by radioimmunoassay (RIA).The effect of citrated platelet poor plasma (PPP) from subjects with renal failure (U-PPP) and healthy age/sex matched controls (C-PPP) on 6-oxo-PGFi,, production were compared.2 No difference was detected between either 6-oxo-PGFia or PGI2 concentration when rings were incubated with U-PPP or C-PPP for 4, 8 and 30 min for 6-oxo-PGFi,a (P > 0.05, n = 8); and 30 min for PGI2 (P > 0.05, n = 8).3 Consistently more 6-oxo-PGFIa was produced in PPP that had been heated at 100°C for S min (H-PPP) than in C-PPP: mean 6-oxo-PGFi,, was increased by factors of 1.45, 1.61, 1.57 and 1.57 at 4, 8, 30 and 60 min respectively (P < 0.005 at each time, n = 8).4 Similar amounts of 6-oxo-PGFia were produced by aortic rings incubated in H-PPP and in Tris buffer (50 mm, pH 7.5), P > 0.05 at all times (n = 8).5 The half-life of PGI2 in U-PPP was similar to that in C-PPP; 7.8 + 0.6 min and 10.2 + 1.9 min (mean + s.e.mean) respectively (P > 0.05).6 In separate experiments a comparison was made of 6-oxo-PGFIa production by aortic rings incubated in C-PPP, H-PPP and H-PPP to which albumin had been added to restore its original concentration.It was confirmed that more 6-oxo-PGFI, was produced in H-PPP than in C-PPP (P < 0.05, n = 4).This increment was abolished in the H-PPP to which albumin had been added. 7It was concluded that the heat-labile inhibitor of vascular PGI2 synthesis in human plasma is albumin.8 The failure to demonstrate a stimulator of PGI2 synthesis in fresh aortic rings by U-PPP does not support the hypothesis that the bleeding diathesis of renal failure is due to an excess of a PGI2 stimulating factor in plasma.