title: Reactivity of brain parenchymal arterioles after ischemia and reperfusion.
abstract: OBJECTIVE
  We investigated the effect of ischemia and reperfusion on the vasoactive function of penetrating brain parenchymal arterioles under pressurized conditions.
  
  
  METHODS
  Parenchymal arterioles (< 50 microm in diameter) from within the middle cerebral artery territory were dissected from male Wistar rats that were either nonischemic control (n = 16) or ischemic for one hour and reperfused for 24 hours (n = 16) by temporary filament occlusion of the middle cerebral artery. Arterioles were mounted on glass cannulas within an arteriograph chamber that allowed for the measurement of lumen diameter and control over intravascular pressure.
  
  
  RESULTS
  After one hour of equilibration at 10 mmHg, spontaneous myogenic tone developed in both groups of animals, constricting control arterioles from 69 +/- 9 to 49 +/- 11 microm (29.5 +/- 10.2%) and ischemic arterioles from 66 +/- 9 to 45 +/- 11 microm (33.1 +/- 14.1%); p > 0.05. Contraction to the nitric oxide synthase inhibitor nitro-L-arginine (10(-4)M) was significantly diminished in ischemic arterioles, constricting only 3.2 +/- 3.3 vs. 15.6 +/- 12.5% in control arterioles (p = 0.017). Both groups dilated to nifedipine; however, the response was significantly diminished after ischemia. The EC50 for nifedipine in control arterioles was 3.54 +/- 0.11 vs. 9.90 +/- 0.71 nM for ischemic arterioles (p = 0.024).
  
  
  CONCLUSIONS
  These findings demonstrate that functional changes occur in brain parenchymal arterioles after ischemia and reperfusion, a result that may significantly influence stroke outcome by altering blood flow to an ischemic region.
authors.affiliation: Department of Neurology, Ob/Gyn and Pharmacology, University of Vermont College of Medicine, Burlington, Vermont 05405, USA. Marilyn.Cipolla@uvm.edu
authors.forename: Marilyn J
authors.initials: MJ
authors.lastname: Cipolla
authors.forename: Lisa V
authors.initials: LV
authors.lastname: Bullinger
mesh_terms: D000818:Animals; D001160:Arterioles / Q000201:enzymology / Q000503:physiopathology; D001921:Brain / Q000098:blood supply* / Q000201:enzymology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000201:enzymology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D020768:Middle Cerebral Artery / Q000201:enzymology / Q000503:physiopathology; D009543:Nifedipine / Q000494:pharmacology; D019001:Nitric Oxide Synthase; D019335:Nitroarginine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000201:enzymology / Q000503:physiopathology*; D020521:Stroke / Q000201:enzymology / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D019335:Nitroarginine; D019001:Nitric Oxide Synthase; D009543:Nifedipine