title: Cholesterol, but not cigarette smoke, decreases rabbit carotid artery relaxation.
abstract: The purpose of this study was to determine the physiologic effects of cigarette smoke exposure and dietary cholesterol on the availability of nitric oxide in carotid vascular rings. New Zealand white rabbits were placed in an airflow chamber for 3 hr/day over an 8-week period and were exposed to smoke from 600 cigarettes/per day added to the chamber inflow by a robotic smoke generator. New Zealand white rabbits, made hypercholesterolemic, and one group fed a normal diet, were similarly placed in the chamber without exposure to cigarette smoke. In those exposed groups, serum cotinine and cholesterol levels were consistently elevated. After the 8-week period, the carotid arteries were harvested. The vessels were cut into 3-mm rings which were suspended from pressure transducers. The rings were contracted with potassium chloride (KCl) to determine vessel integrity. One ring from each carotid was maximally contracted with 1 x 10(-3) molar norepinephrine (NE) while the experimental ring was contracted to 50% of maximum. Relaxation of the rings was achieved by adding incremental doses of acetylcholine. Our results showed that endothelial dysfunction, as measured by acetylcholine-mediated vasorelaxation, occurs in the rabbit carotid artery when exposed to high dietary cholesterol. Cigarette exposure alone in this particular vessel did not result in significant alteration in acetylcholine-mediated vasorelaxation.
authors.affiliation: Department of Vascular Surgery, Medical College of Wisconsin and Surgical Services, Zablocki VA Medical Center, Milwaukee, WI, USA.
authors.forename: D
authors.initials: D
authors.lastname: Johnson
authors.forename: J A
authors.initials: JA
authors.lastname: Freischlag
authors.forename: D A
authors.initials: DA
authors.lastname: Coe
authors.forename: J H
authors.initials: JH
authors.lastname: Mudaliar
authors.forename: D K
authors.initials: DK
authors.lastname: Traul
authors.forename: H
authors.initials: H
authors.lastname: Kelly
authors.forename: L
authors.initials: L
authors.lastname: Hanson
authors.forename: R A
authors.initials: RA
authors.lastname: Cambria
authors.forename: G R
authors.initials: GR
authors.lastname: Seabrook
authors.forename: J B
authors.initials: JB
authors.lastname: Towne
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000009:adverse effects; D003367:Cotinine / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006937:Hypercholesterolemia / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D010947:Plants, Toxic; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D012906:Smoke / Q000009:adverse effects; D012907:Smoking / Q000503:physiopathology*; D014026:Nicotiana / Q000009:adverse effects; D014160:Transducers, Pressure; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology*; D014665:Vasodilator Agents / Q000378:metabolism / Q000494:pharmacology
chemical_list: D002791:Cholesterol, Dietary; D012906:Smoke; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D011189:Potassium Chloride; D002784:Cholesterol; D003367:Cotinine; D000109:Acetylcholine; D009638:Norepinephrine