title: Single LDL apheresis improves endothelium-dependent vasodilatation in hypercholesterolemic humans.
abstract: BACKGROUND
  Although long-term lipid-lowering therapy improves endothelium-dependent vasodilatation in humans, it remains unknown whether the short-term removal of LDL per se ameliorates endothelial dysfunction.
  
  
  RESULTS
  To examine the effects 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 single LDL apheresis while infusing acetylcholine (ACh; 4 to 24 micrograms/min) and sodium nitroprusside (SNP; 0.2 to 1.2 micrograms/min). The single session of LDL apheresis reduced total LDL (from 142.2 +/- 15.0 to 32.6 +/- 5.0 mg/mL, P < .0005) and oxidized LDL (from 111.6 +/- 22.8 to 30.0 +/- 5.4 ng/mL, P < .005). Although ACh and SNP increased FBF dose-dependently before and after LDL apheresis, the endothelium-dependent vasodilatation responses to ACh were significantly augmented (P < .01) after the single session of LDL apheresis without changes in the endothelium-independent vasodilatation responses to SNP. The plasma levels of total and oxidized LDL correlated with the degree of ACh-induced vasodilatation. Furthermore, the local production of nitrate/nitrite, metabolites of NO, during ACh infusion was significantly (P < .05) augmented by LDL apheresis, and there was a significant correlation between the degree of ACh-induced vasodilatation and the production in nitrate/nitrite (r = .99, P < .0005).
  
  
  CONCLUSIONS
  We demonstrated that even a single session of LDL apheresis with the reduction of total LDL and oxidized LDL improved endothelial function. Our results suggest that total LDL and/or oxidized LDL may directly impair endothelial function in the human forearm vessel.
authors.affiliation: Department of Internal Medicine III, Kurume University School of Medicine, Fukuoka, Japan.
authors.forename: O
authors.initials: O
authors.lastname: Tamai
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: H
authors.initials: H
authors.lastname: Itabe
authors.forename: Y
authors.initials: Y
authors.lastname: Wada
authors.forename: K
authors.initials: K
authors.lastname: Kohno
authors.forename: T
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D001781:Blood Component Removal; D008078:Cholesterol, LDL / Q000097:blood*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000209:etiology; D009569:Nitric Oxide / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects
chemical_list: D008078:Cholesterol, LDL; D009599:Nitroprusside; D009569:Nitric Oxide; D000109:Acetylcholine