title: In vitro protection of vascular function from oxidative stress and inflammation by pulsatility in resistance arteries.
abstract: OBJECTIVE
  Resistance arteries remain subject to pulsatility, a potent regulator of large elastic artery tone and structure, but the effect is incompletely understood. Extracorporeal circulation during cardiac surgery is often associated with absence of pulsatility, which may affect vascular tone. To define the role of the vascular wall in the inflammatory process that may occur with or without pulsatility, we studied resistance arteries functions ex vivo. We measured vascular reactivity, oxidative stress, and inflammation in the arterial wall.
  
  
  METHODS
  Isolated rat mesenteric resistance arteries were mounted in an arteriograph and subjected to pulsatility or not in vitro. Arteries were perfused with a physiologic salt solution without circulating cells.
  
  
  RESULTS
  After 180 minutes, flow-mediated dilation was higher and pressure-induced myogenic tone lower in arteries subjected to pulsatility. Without pulsatility, reactive oxygen species and markers of inflammation (monocyte chemotactic protein 1 and tumor necrosis factor α) were higher than baseline. In perfused mesenteric beds under similar conditions, tumor necrosis factor α was higher in perfusate after 180 minutes of nonpulsatility (5.7 ± 1.6 pg/mL vs 1.1 ± 0.4 pg/mL; P < .01). In arteries treated with the antioxidant 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (tempol), flow-mediated dilation and myogenic tone were similar in nonpulsatile and pulsatile arteries; monocyte chemotactic protein 1 and nuclear factor κB expression levels were not increased in tempol-treated nonpulsatile arteries.
  
  
  CONCLUSIONS
  Absence of pulsatility in resistance arteries increased oxidative stress, which in turn induced inflammation and preferentially altered pressure and flow-dependent tone, which play a key role in control of local blood flow.
authors.affiliation: Centre Hospitalier Universitaire d'Angers, Angers, France.
authors.forename: Frédéric
authors.initials: F
authors.lastname: Pinaud
authors.forename: Laurent
authors.initials: L
authors.lastname: Loufrani
authors.forename: Bertrand
authors.initials: B
authors.lastname: Toutain
authors.forename: Diane
authors.initials: D
authors.lastname: Lambert
authors.forename: Lionel
authors.initials: L
authors.lastname: Vandekerckhove
authors.forename: Daniel
authors.initials: D
authors.lastname: Henrion
authors.forename: Christophe
authors.initials: C
authors.lastname: Baufreton
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001794:Blood Pressure; D018932:Chemokine CCL2 / Q000378:metabolism; D003497:Cyclic N-Oxides / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D018384:Oxidative Stress; D011673:Pulsatile Flow; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013113:Spin Labels; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D000975:Antioxidants; C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D003497:Cyclic N-Oxides; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species; D013113:Spin Labels; D014409:Tumor Necrosis Factor-alpha; C001803:tempol