Oxidative stress during hemodialysis: Effect of heparin

Abstract

Patients on chronic hemodialysis (HD) are exposed to oxidative stress. An HD session is used in this study as an in vivo model for studying the influence of heparin on oxidative stress caused partially by activated peripheral blood polymorphonuclear leukocytes (PMNLs) during a HD session. Each patient underwent HD once with and once without heparin. Oxidative stress was determined by evaluating both the rate of superoxide release from phorbol 12-myristate 13-acetate (PMA)-stimulated PMNLs and plasma levels of oxidized glutathione (GSSG), both measured before and after the dialysis session. In vitro, heparin reduced the rate of superoxide release from separated PMA-stimulated PMNLs. In vivo, the rate of superoxide release from PMNLs was always increased after the dialysis session, regardless of the presence of heparin. However, in the presence of heparin, this increase was significantly smaller. The augmentation in the rate of superoxide release after the dialysis session without heparin was accompanied by a significant elevation of GSSG, reflecting a preceding oxidation of plasma glutathione. The increase in both parameters, the rate of superoxide release, and the plasma GSSG concentration after HD treatment suggest that heparin in vivo alleviates the oxidative stress induced by the dialysis process. Based on our results, heparin should be the anticoagulant of choice because of its suppressant action on HD-induced oxidative stress.