title: Enhancement of endothelial function inhibits left atrial thrombi development in an animal model of spontaneous left atrial thrombosis.
abstract: BACKGROUND
  Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.
  
  
  RESULTS
  Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats.
  
  
  CONCLUSIONS
  They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis.
authors.affiliation: Department of Nutrition and Metabolism, Institute of Health Biosciences, the University of Tokushima Graduate School.
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Mawatari
authors.forename: Emiko
authors.initials: E
authors.lastname: Yoshioka
authors.forename: Satomi
authors.initials: S
authors.lastname: Toda
authors.forename: Sonoko
authors.initials: S
authors.lastname: Yasui
authors.forename: Hiroko
authors.initials: H
authors.lastname: Furukawa
authors.forename: Takaaki
authors.initials: T
authors.lastname: Shimohata
authors.forename: Takamasa
authors.initials: T
authors.lastname: Ohnishi
authors.forename: Masaki
authors.initials: M
authors.lastname: Morishima
authors.forename: Nagakatsu
authors.initials: N
authors.lastname: Harada
authors.forename: Akira
authors.initials: A
authors.lastname: Takahashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sakaue
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Nakaya
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004727:Endothelium / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006325:Heart Atria / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D051381:Rats; D013927:Thrombosis / Q000378:metabolism* / Q000473:pathology
chemical_list: D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat