title: Postischemic augmentation of conducted dilation in cerebral arterioles.
abstract: OBJECTIVE
  Conducted vasomotor responses likely play an important role in cerebrovascular regulation, but it is unclear how these responses may be affected by ischemia. The purpose of this study was to evaluate the hypothesis that cerebral ischemia and reperfusion (I/R) alters vascular conduction in cerebral arterioles.
  
  
  METHODS
  Middle cerebral artery occlusion (MCAO) was induced by an intraluminal filament technique in 4 groups of rats: (A) 2-hour MCAO/24-hour reperfusion (n=14); (B) 2-hour MCAO/1-hour reperfusion (n=7); (C) 1-hour MCAO/24-hour reperfusion (n=6); and (D) 1-hour MCAO/1-hour reperfusion (n=5). Neurological status and infarction (2,3,5-triphenyltetrazolium chloride staining) were evaluated after I/R. Conducted vasomotor responses were assessed in intracerebral branches of the MCA, by following the longitudinal spread of vasodilation or vasoconstriction to localized microapplication of ATP or adenosine.
  
  
  RESULTS
  Local microapplication of ATP evoked a biphasic constriction (17+/-3%) and dilation (7+/-2%) response, whereas adenosine elicited only dilation (11+/-2%). These local responses spread longitudinally along sham-control arterioles (1 mm conduction distance) with rapid spatial decay. Ischemia followed by 24-hour reperfusion (groups A and C) led to a marked potentiation of conducted dilation responses: dilation to ATP conducted with virtually no decay in I/R arterioles. Augmentation of conductivity was not observed in the 1-hour reperfusion groups (B and D). Moreover, I/R did not alter conducted constriction.
  
  
  CONCLUSIONS
  Ischemia-reperfusion led to a specific augmentation of conducted vasodilation in cerebral arterioles. Presumably, enhanced conductivity may improve cerebral perfusion after ischemia.
authors.affiliation: Department of Neurological Surgery, University of Washington School of Medicine, Seattle, WA 98104-2499. ngai@u.washington.edu
authors.forename: Al C
authors.initials: AC
authors.lastname: Ngai
authors.forename: Thien-Son
authors.initials: TS
authors.lastname: Nguyen
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Meno
authors.forename: Gavin W
authors.initials: GW
authors.lastname: Britz
mesh_terms: D000241:Adenosine / Q000378:metabolism / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000503:physiopathology*; D013778:Tetrazolium Salts; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D013778:Tetrazolium Salts; C009591:triphenyltetrazolium; D000255:Adenosine Triphosphate; D000241:Adenosine