title: Effects of dietary flaxseed on vascular contractile function and atherosclerosis during prolonged hypercholesterolemia in rabbits.
abstract: Dietary flaxseed has significant anti-atherogenic effects. However, the limits of this action and its effects on vascular contractile function are not known. We evaluated the effects of flaxseed supplementation on atherosclerosis and vascular function under prolonged hypercholesterolemic conditions in New Zealand White rabbits assigned to one of four groups for 6, 8, or 16 wk of feeding: regular diet (RG), 10% flaxseed-supplemented diet (FX), 0.5% cholesterol-supplemented diet (CH), and 0.5% cholesterol- and 10% flaxseed-supplemented diet (CF). Cholesterol feeding resulted in elevated plasma cholesterol levels and the development of atherosclerosis. The CF group had significantly less atherosclerotic lesions in the aorta and carotid arteries after 6 and 8 wk than the CH animals. However, the anti-atherogenic effect of flaxseed supplementation was completely attenuated by 16 wk. Maximal tension induced in aortic rings either by KCl or norepinephrine was not impaired by dietary cholesterol until 16 wk. This functional impairment was not prevented by including flaxseed in the high-cholesterol diet. Aortic rings from the cholesterol-fed rabbits exhibited an impaired relaxation response to acetylcholine at all time points examined. Including flaxseed in the high-cholesterol diet completely normalized the relaxation response at 6 and 8 wk and partially restored it at 16 wk. No significant changes in the relaxation response induced by sodium nitroprusside were observed in any of the groups. In summary, dietary flaxseed is a valuable strategy to limit cholesterol-induced atherogenesis as well as abnormalities in endothelial-dependent vasorelaxation. However, these beneficial effects were attenuated during prolonged hypercholesterolemic conditions.
authors.affiliation: Canadian Centre for Agri-Food Research in Health and Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
authors.forename: C M C
authors.initials: CM
authors.lastname: Dupasquier
authors.forename: A-M
authors.initials: AM
authors.lastname: Weber
authors.forename: B P
authors.initials: BP
authors.lastname: Ander
authors.forename: P P
authors.initials: PP
authors.lastname: Rampersad
authors.forename: S
authors.initials: S
authors.lastname: Steigerwald
authors.forename: J T
authors.initials: JT
authors.lastname: Wigle
authors.forename: R W
authors.initials: RW
authors.lastname: Mitchell
authors.forename: E A
authors.initials: EA
authors.lastname: Kroeger
authors.forename: J S C
authors.initials: JS
authors.lastname: Gilchrist
authors.forename: M M
authors.initials: MM
authors.lastname: Moghadasian
authors.forename: A
authors.initials: A
authors.lastname: Lukas
authors.forename: G N
authors.initials: GN
authors.lastname: Pierce
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology / Q000503:physiopathology; D002339:Carotid Arteries / Q000473:pathology / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000494:pharmacology; D003324:Coronary Artery Disease / Q000178:diet therapy* / Q000473:pathology / Q000503:physiopathology*; D019587:Dietary Supplements; D005227:Fatty Acids / Q000097:blood; D019597:Flax; D006937:Hypercholesterolemia / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D011817:Rabbits; D014280:Triglycerides / Q000097:blood; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D002791:Cholesterol, Dietary; D005227:Fatty Acids; D014280:Triglycerides; D014665:Vasodilator Agents; D009599:Nitroprusside; D002784:Cholesterol