title: Nitric oxide promotes arteriolar dilation during cortical spreading depression in rabbits.
abstract: OBJECTIVE
  Pial arterioles transiently dilate during cortical spreading depression (CSD), although the mechanisms are unclear. We tested the hypothesis that increased production of nitric oxide (NO) promotes arteriolar dilation.
  
  
  METHODS
  Urethane-anesthetized rabbits were equipped with cranial windows, and the diameter (reported in micrometers) of a pial arteriole was determined via intravital microscopy. In each rabbit, a baseline CSD was elicited by microapplication of KCl onto the cortex, and resultant pial arteriolar dilation was measured. Either 100 mumol/L N omega-nitro-L-arginine methyl ester (L-NAME) or 50 mumol/L NG-nitro-L-arginine (L-NA), both competitive NO synthase inhibitors, was then applied to the brain surface. A CSD was elicited as before. The L-NAME and L-NA were then removed by artificial cerebrospinal fluid washes. An additional CSD was induced with KCl as before.
  
  
  RESULTS
  Control CSD in the L-NAME group dilated pial arterioles; baseline diameter, 66 +/- 7 mm, with CSD = 106 +/- 8 mm (59% increase). After topically applied L-NAME, CSD dilated pial arterioles less: baseline diameter, 61 +/- 7 mm, with CSD = 77 +/- 6 mm (26% increase), P < .05 compared with control CSD diameter. Topical L-NA had similar effects on CSD: control CSD dilated pial arterioles 51%; after topical L-NA, only 14% (P < .05). After removal of L-NAME or L-NA, CSD-induced pial arteriolar dilation was similar to original control values.
  
  
  CONCLUSIONS
  The reversible inhibition of CSD-induced pial arteriolar dilation by either L-NAME or L-NA suggests that NO contributes to arteriolar dilation observed with CSD.
authors.affiliation: Department of Anesthesia, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1009.
authors.forename: D M
authors.initials: DM
authors.lastname: Colonna
authors.forename: W
authors.initials: W
authors.lastname: Meng
authors.forename: D D
authors.initials: DD
authors.lastname: Deal
authors.forename: D W
authors.initials: DW
authors.lastname: Busija
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000241:Adenosine / Q000494:pharmacology; D000287:Administration, Topical; D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D001160:Arterioles / Q000187:drug effects; D013181:Cortical Spreading Depression / Q000187:drug effects*; D005260:Female; D009252:NADPH Dehydrogenase / Q000037:antagonists & inhibitors; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D019001:Nitric Oxide Synthase; D019335:Nitroarginine; D010841:Pia Mater / Q000098:blood supply* / Q000187:drug effects*; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000037:antagonists & inhibitors / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D019335:Nitroarginine; D009569:Nitric Oxide; D011189:Potassium Chloride; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D009252:NADPH Dehydrogenase; D000241:Adenosine; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester