title: Direct effects of triiodothyronine on human internal mammary artery and saphenous veins.
abstract: OBJECTIVE
  Thyroid hormone (3,5,3'-triiodo-L-thyronine is under investigation as a positive inotrope and vasodilator for patients undergoing cardiac surgery. This study determined the direct effects of triiodothyronine on human blood vessels.
  
  
  METHODS
  Prospective, controlled, in vitro study.
  
  
  METHODS
  Laboratory facility in a university teaching hospital.
  
  
  METHODS
  Small excess segments of internal mammary arteries or saphenous veins were obtained from patients undergoing coronary artery bypass surgery.
  
  
  METHODS
  Vessel segments were cut into rings to measure isometric tension development in isolated tissue baths containing Krebs-Ringer bicarbonate solution at 37 degrees C. Rings were prestretched in vitro to resting tensions analogous to mean arterial or central venous pressures in vivo and then constricted with potassium or phenylephrine. Rings were exposed to increasing concentrations of triiodothyronine (4 x 10(-12) to 1 x 10(-4) mol/L) to obtain dose-response curves.
  
  
  RESULTS
  High concentrations (> or = 3.3 x 10(-5) mol/L) of trilodothyronine produced dose-dependent relaxation of preconstricted rings. The relaxation was not selective for arteries or veins at arterial resting tensions, and with either potassium or phenylephrine as a vasoconstrictor. Propranolol had little effect on subsequent triiodothyronine-induced relaxation of potassium-constricted rings at resting arterial tensions.
  
  
  CONCLUSIONS
  Triiodothyronine, in supraphysiological and suprapharmacological concentrations, dilates preconstricted rings of human blood vessels in vitro; however, triiodothyronine had no demonstrable vasomotor effects on human internal mammary artery or saphenous vein in clinically relevant concentrations (10(-9) to 10(-8) mol/L). Triiodothyronine administration in vivo most likely has little direct effect on the tone of human vascular smooth muscle, particularly coronary artery bypass conduits.
authors.affiliation: Department of Anesthesiology, Temple University Hospital, Philadelphia, PA 19140, USA.
authors.forename: L J
authors.initials: LJ
authors.lastname: Krasner
authors.forename: W W
authors.initials: WW
authors.lastname: Wendling
authors.forename: S C
authors.initials: SC
authors.lastname: Cooper
authors.forename: D
authors.initials: D
authors.lastname: Chen
authors.forename: S K
authors.initials: SK
authors.lastname: Hellmann
authors.forename: C J
authors.initials: CJ
authors.lastname: Eldridge
authors.forename: J B
authors.initials: JB
authors.lastname: McClurken
authors.forename: V
authors.initials: V
authors.lastname: Jeevanandam
authors.forename: C
authors.initials: C
authors.lastname: Carlsson
mesh_terms: D001794:Blood Pressure / Q000187:drug effects; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002496:Central Venous Pressure / Q000187:drug effects; D001026:Coronary Artery Bypass; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007537:Isometric Contraction / Q000187:drug effects; D007552:Isotonic Solutions; D008323:Mammary Arteries / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011446:Prospective Studies; D012501:Saphenous Vein / Q000187:drug effects*; D014284:Triiodothyronine / Q000008:administration & dosage / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*; D014666:Vasomotor System / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D007552:Isotonic Solutions; C051865:Krebs-Ringer solution; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D014284:Triiodothyronine; D010656:Phenylephrine; D011433:Propranolol; D011188:Potassium