title: Transmyocardial laser treatment denervates canine myocardium.
abstract: BACKGROUND
  In patients with refractory angina who are not candidates for conventional revascularization, transmyocardial laser treatment reduces angina significantly in the early postoperative period. We hypothesized that transmyocardial laser treatment damages cardiac nerve fibers that convey the pain of angina pectoris.
  
  
  METHODS
  Left thoracotomy was performed in sixteen adult mongrel dogs. Treatment groups included animals in which a portion of the left ventricle underwent creation of transmyocardial channels with a holmium:yttrium-aluminum-garnet laser (n = 5) or chemical destruction of cardiac nerves by application of phenol to the epicardium (n = 5). Sham-operated negative control animals underwent thoracotomy and pericardiotomy alone (n = 6). Cardiac afferent nerve function was assessed by epicardial application of bradykinin, a potent algesic, before treatment and 2 weeks after the operation. The resulting central nervous system-mediated decrease in systemic mean arterial pressure was measured. Cardiac innervation of treated and untreated left ventricular myocardium was further assessed by immunoblot analysis performed with an antibody against tyrosine hydroxylase, a sympathetic nerve-specific enzyme.
  
  
  RESULTS
  Before treatment, changes in systemic arterial pressure were seen with bradykinin stimulation in all dogs. Two weeks after treatment, no hemodynamic response was seen after stimulation of laser- or phenol-treated areas, but a normal response was seen after stimulation of untreated areas in these same animals and in negative control animals. Immunoblots demonstrated loss of tyrosine hydroxylase in regions of phenol and laser treatment.
  
  
  CONCLUSIONS
  Transmyocardial laser treatment destroys cardiac nerve fibers, which may contribute to the reduced angina pectoris seen clinically.
authors.affiliation: Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: K F
authors.initials: KF
authors.lastname: Kwong
authors.forename: G K
authors.initials: GK
authors.lastname: Kanellopoulos
authors.forename: J C
authors.initials: JC
authors.lastname: Nickols
authors.forename: S M
authors.initials: SM
authors.lastname: Pogwizd
authors.forename: J E
authors.initials: JE
authors.lastname: Saffitz
authors.forename: R B
authors.initials: RB
authors.lastname: Schuessler
authors.forename: T M
authors.initials: TM
authors.lastname: Sundt
mesh_terms: D000787:Angina Pectoris / Q000503:physiopathology / Q000601:surgery; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001920:Bradykinin / Q000494:pharmacology; D004285:Dogs; D006321:Heart / Q000294:innervation*; D006801:Humans; D015151:Immunoblotting; D053685:Laser Therapy; D009206:Myocardium / Q000201:enzymology; D009412:Nerve Fibers / Q000502:physiology; D013562:Sympathectomy / Q000379:methods; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D014446:Tyrosine 3-Monooxygenase; D001920:Bradykinin