title: Impaired exercise-induced vasodilatation in chronic atrial fibrillation--role of endothelium-derived nitric oxide.
abstract: Exercise capacity is often reduced in patients with atrial fibrillation (AF), but very few studies have focused on changes in endothelial function as a potential mechanism for the exercise limitation. The present study used using venous occlusion plethysmography to investigate whether nitric oxide (NO)-mediated vasodilatation is attenuated during exercise in patients with AF by measuring forearm blood flow (FBF) in 10 patients at rest and immediately after 2 levels of rhythmic handgrip exercise, before and after inhibition of NO synthesis with N(G)-monomethyl-L-arginine (L-NMMA, 100 micromol). The measurements were repeated 1 day after restoration of sinus rhythm by cardioversion. FBF responses to graded doses of acetylcholine (ACh) were also observed before and after cardioversion. Heart rate decreased after cardioversion, but blood pressure did not change. FBF at rest was not affected by cardioversion, but at the highest level of exercise it increased from 28.4+/-2.3 ml x min(-1) x dl(-1) before to 39.4+/-3.2 ml x min(-1) x dl(-1) after cardioversion (p<0.05). L-NMMA significantly decreased FBF at rest (p<0.01) and depressed the increase in FBF response to exercise after (p<0.01), but not before cardioversion. The FBF response to ACh was also accelerated significantly after cardioversion. The present results provide new evidence that NO bioavailability is depressed at rest and during exercise in patients with AF.
authors.affiliation: Fourth Department of Internal Medicine, Shimane Medical University, Izumo, Japan.
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Ishibashi
authors.forename: Toshio
authors.initials: T
authors.lastname: Shimada
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sakane
authors.forename: Shuzo
authors.initials: S
authors.lastname: Ohata
authors.forename: Takashi
authors.initials: T
authors.lastname: Sugamori
authors.forename: Yoko
authors.initials: Y
authors.lastname: Ohta
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Inoue
authors.forename: Ko
authors.initials: K
authors.lastname: Nakamura
authors.forename: Hiromi
authors.initials: H
authors.lastname: Shimizu
authors.forename: Harumi
authors.initials: H
authors.lastname: Katoh
authors.forename: Yo
authors.initials: Y
authors.lastname: Murakami
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002908:Chronic Disease; D004554:Electric Countershock; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D005542:Forearm / Q000098:blood supply; D018737:Hand Strength; D006331:Heart Diseases / Q000150:complications / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology*; D010991:Plethysmography; D014664:Vasodilation / Q000502:physiology*; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D000109:Acetylcholine