title: Direct effects of alpha1- and alpha2-adrenergic agonists on spinal and cerebral pial vessels in dogs.
abstract: BACKGROUND
  The effects of adrenergic agonists, often used as local anesthetic additives or spinal analgesics, on spinal vessels have not been firmly established. The authors investigated the effects of alpha2- and alpha1-adrenergic agonists on spinal and cerebral pial vessels in vivo.
  
  
  METHODS
  Pentobarbital-anesthetized dogs (n = 28) were prepared for measurement of spinal pial-vessel diameter in a spinal-window preparation. The authors applied dexmedetomidine, clonidine, phenylephrine, or epinephrine in three different concentrations (0.5, 5.0, and 50 microg/ml; [2.1, 1.9, 2.5, and 2.3] x [10(-6), 10(-5), and 10(-4)] M, respectively) under the window (one drug in each dog) and measured spinal pial arteriolar and venular diameters in a sequential manner. To enable the comparison of their effects on cerebral vessels, the authors also administered these drugs under a cranial window.
  
  
  RESULTS
  On topical administration, each drug constricted spinal pial arterioles in a concentration-dependent manner. Phenylephrine and epinephrine induced a significantly larger arteriolar constriction than dexmedetomidine or clonidine at 5 microg/ml (8%, 11%, 0%, and 1%, respectively). Spinal pial venules tended to be less constricted than arterioles. In cerebral arterioles, greater constrictions were induced by dexmedetomidine and clonidine than those induced by phenylephrine and epinephrine (14%, 8%, 0%, and 1%, respectively). Cerebral pial venules tended to exhibit larger constrictions than cerebral arterioles (unlike in spinal vessels).
  
  
  CONCLUSIONS
  Dexmedetomidine and clonidine constricted spinal vessels in a concentration-dependent manner, but such vasoconstrictions were smaller than those induced by phenylephrine and epinephrine.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Gifu University School of Medicine, Gifu City, Japan. iida@cc.gifu-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Iida
authors.forename: H
authors.initials: H
authors.lastname: Ohata
authors.forename: M
authors.initials: M
authors.lastname: Iida
authors.forename: Y
authors.initials: Y
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Dohi
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists; D058647:Adrenergic alpha-2 Receptor Agonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects; D001921:Brain / Q000098:blood supply*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003000:Clonidine / Q000494:pharmacology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D020926:Medetomidine; D010656:Phenylephrine / Q000494:pharmacology; D013116:Spinal Cord / Q000098:blood supply*; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D058647:Adrenergic alpha-2 Receptor Agonists; D000316:Adrenergic alpha-Agonists; D007093:Imidazoles; D010656:Phenylephrine; D003000:Clonidine; D020926:Medetomidine; D004837:Epinephrine