title: Nitric oxide and prostacyclin in ultrasonic vasodilatation of the canine internal mammary artery.
abstract: BACKGROUND
  Investigators recently demonstrated increased free blood flow from radial artery free grafts harvested using ultrasonic technology. We investigated the mechanism underlying this phenomenon.
  
  
  METHODS
  Canine internal mammary artery segments (with and without intact endothelium) were precontracted with norepinephrine and sonicated 3 seconds in organ chambers with ultrasonic coagulating shears (Harmonic Scalpel; Ethicon Endo-Surgery, Cincinnati, OH) functioning at level 2. Vessel tension was continuously measured to examine vasoactivity in response to sonication alone (control) or with N(ù)-Nitro-l-arginine (l-NNA) and indomethacin added to the chamber medium individually or in combination. Tissue heating, acoustic pressure, and endothelial damage as detected by scanning electron micrography were also assessed.
  
  
  RESULTS
  In vitro sonication with the Harmonic Scalpel induced predominately endothelium-dependent internal mammary artery vasorelaxation but a small endothelium-independent contribution was also observed. Early vasorelaxation (1 minute after stimulus) was maximally inhibited by l-NNA alone and in combination with indomethacin. Relaxation during this period was insignificantly affected by indomethacin alone. Only the combination of l-NNA and indomethacin maximally inhibited late vasorelaxation (5 minutes after stimulus), whereas inhibitory effects of l-NNA diminished during this time period. Indomethacin inhibited relaxation substantially during this phase, although significantly less than did l-NNA alone. The Harmonic Scalpel minimally heated the tissue surface (0.3 +/- 0.03 degrees C) and did not disrupt endothelial cell integrity while operating at 50 mW/cm(2) intensity (acoustic pressure 40 kPa).
  
  
  CONCLUSIONS
  Sonication induces vasorelaxation almost completely by time-dependent endothelial nitric oxide and prostacyclin release, which appears unrelated to tissue heating or endothelial architectural disruption.
authors.affiliation: Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota 55905, USA.
authors.forename: Ayako
authors.initials: A
authors.lastname: Maruo
authors.forename: Chad E
authors.initials: CE
authors.lastname: Hamner
authors.forename: Alfredo J
authors.initials: AJ
authors.lastname: Rodrigues
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Higami
authors.forename: James F
authors.initials: JF
authors.lastname: Greenleaf
authors.forename: Hartzell V
authors.initials: HV
authors.lastname: Schaff
mesh_terms: D000818:Animals; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D008297:Male; D008323:Mammary Arteries / Q000187:drug effects* / Q000502:physiology*; D009569:Nitric Oxide / Q000494:pharmacology*; D014465:Ultrasonics; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D009569:Nitric Oxide; D011464:Epoprostenol