Changes of Arterial Prostaglandin E2 During Haemodialysis

Abstract

The absence of a reduction in peripheral vascular resistance secondary to hypervolaemia leads to so-called volume hypertension. In order to study whether a deficient formation of the vasodilator autacoid prostaglandin E2 (PGE2) contributes to the preservation of inadequate vascular tone during extracellular volume expansion, arterial plasma PGE2 and the stable PGE2 metabolite 13,14-dihydro-15-keto-PGE2 (PGE2-M) were determined in 13 oligoanuric women on chronic haemodialysis. Prior to treatment eight of them had hypervolaemia and hypertension (mean arterial pressure (MAP) 128 +/- 3 mmHg (mean +/- SE] and five patients had hypervolaemia of a similar degree but were not hypertensive (MAP: 99 +/- 4 mmHg P less than 0.005). Before haemodialysis the arterial PGE2 and PGE2-M concentrations were less (P less than 0.05) in hypertensive (11 observations in eight patients) than in normotensive patients (ten observations in five patients). As blood pressure decreased during the course of haemodialysis of volume hypertensive patients, the concentration of PGE2 and PGE2-M increased (P less than 0.02) by 104 +/- 43% and 89 +/- 32%, respectively. In normotensive patients neither blood pressure nor the concentration of PGE2 and PGE2-M were found to change during treatment. Since volume hypertension was associated with reduced values and dialysis induced normalisation of blood pressure with increased arterial values of PGE2 and PGE2-M, we hypothesise that the development of hypertension associated with fluid overload of haemodialysed patients may be related to a decreased release of prostaglandin E2.

Hemodialysis and biotransformation of erythrocyte epoxy fatty acids in peripheral tissue

“…Nonetheless, it is unknown whether RBCs are capable of liberating PUFA hydroxy metabolites into blood or tissues. Previous studies detected small changes in plasma levels of prostaglandin E2 (PGE2), prostaglandin F2a (PGF2a) [41,42] and 5/12-HETE [43] after hemodialysis. Our data demonstrate that LOX metabolites are exhausted (positive arteriovenous difference) in RBCs that pass through the peripheral tissues, specifically the muscles in the upper limbs, during hemodialysis.…”

Effects of hemodialysis on plasma oxylipins

“…We have no evidence that hemodialysis affected resolvins, prostaglandins, thromboxanes, or other LOX/CYP ω/(ω-1)-hydroxylase metabolites in our patients (Shelmadine, 2017). Only few studies detected small changes in PGE2 or PGF2a (Losonczy, 1990;Schultze, 1984) and 5/12-HETE levels (Dolegowska, 2012) 4-HDHA is a mediator of antiangiogenic effects of n-3 PUFAs (Sapieha, 2011). Since we found that the majority of LOX metabolites measured were not affected by dialysis, we suggest that these metabolites are unlikely to play important roles in this scenario.…”