The imbalance in pro- and
anti-oxidant activity causes endothelial dysfunction, which precedes and exacerbates
atherosclerosis.
LDL-
apheresis improves ischemic symptom in patients with
hypercholesterolemia and regresses
atherosclerosis. Whereas, patients who undergo
hemodialysis experience accelerated
atherosclerosis and premature death even though their
cholesterol level is known to be normal. We investigated the association between oxidative modification and endothelial function during a single session of blood purification
therapies,
LDL-
apheresis and
hemodialysis. To examine the effect of a single session of
LDL-
apheresis on endothelial function in patients with
hypercholesterolemia, we measured forearm blood flow (FBF) by strain gauge plethysmography before and after
LDL-
apheresis, while infusing
acetylcholine (ACh) and
sodium nitroprusside (SNP). The single session of
LDL-
apheresis reduced
oxidized-LDL. Although ACh and SNP increased FBF dose-dependently before and after
LDL-
apheresis, ACh response was significantly augmented without changes in responses to SNP. The plasma level of
oxidized LDL correlated with the degree of ACh-induced vasodilatation. To examine the effect of a single session of
hemodialysis on endothelial function in patients with
end stage renal disease, we estimated flow-mediated vasodilation (FMD) during
reactive hyperemia using a high-resolution ultrasonography, before and after a single session of
hemodialysis. We also investigated the effect of anti-oxidative modification during
hemodialysis using an a-
tocopherol acetate-coated or a non-coated
cellulose dialyzer. Non-specific endothelium independent vasodilation was measured after sublingual glyceryltrinitrate spray (GTN; 0.3 mg) administration in each session. A single session of
hemodialysis increased plasma level of
oxidized LDL. Although
hemodialysis treatment did not affect GTN-induced vasodilation, a single session of
hemodialysis impaired the endothelium-dependent vasodilation. Treatment with
vitamin E-coated-dialyzer restored endothelium-dependent vasodilation, which was accompanied by decrease in
oxidized LDL. Thus, endothelial function was impaired by acute increase in oxidative stress and was restored by
anti-oxidant therapy. Our results suggest the importance of controlling oxidative stress in addition to classical risk factors to preserve human endothelial function.