title: Perivascular adipose tissue modulates vascular function in the human internal thoracic artery.
abstract: OBJECTIVE
  Recent studies have shown that perivascular adipose tissue from the rat aorta secretes a substance that can dilate the aorta. The purpose of the present study was to examine whether this vasodilator is also present in human internal thoracic arteries.
  
  
  METHODS
  Vascular function of human internal thoracic arteries with and without perivascular adipose tissue was assessed with wire myography, and morphology was examined with light microscopy.
  
  
  RESULTS
  The presence of perivascular adipose tissue attenuated the maximal contraction to U 46619 and the contraction to phenylephrine (1 micromol/L) by 37% and 24%, respectively. Transfer of the solution incubated with a perivascular adipose tissue-intact vessel (donor) to a vessel without perivascular adipose tissue (recipient) induced a significant relaxation (36%) in the recipient artery precontracted with phenylephrine. Transfer of incubation solution with perivascular adipose tissue alone also induced a relaxation response in the recipient vessel (37%). The relaxation of the recipient artery induced by the transfer of incubation solution from the donor (artery with intact perivascular adipose tissue or perivascular adipose tissue alone) was absent in vessels precontracted by KCl (60 mmol/L) and was prevented by calcium-dependent potassium channel blockers (tetraethylammonium chloride, 1 mmol/L; iberiotoxin, 100 nmol/L), but not by the voltage-dependent potassium channel blocker 4-aminopyridine (1 mmol/L) and the adenosine triphosphate-dependent potassium channel blocker glibenclamide (10 micromol/L).
  
  
  CONCLUSIONS
  Perivascular adipose tissue in human internal thoracic arteries releases a transferable relaxation factor that acts through the activation of calcium-dependent potassium channels. Because perivascular adipose tissue is often removed in coronary artery bypass grafting, retaining perivascular adipose tissue might be helpful in reducing the occurrence of vasospasm of the graft vessels.
authors.affiliation: Department of Anaesthesia, McMaster University, Hamilton, Ontario, Canada. gaoyu@mcmaster.ca
authors.forename: Yu-Jing
authors.initials: YJ
authors.lastname: Gao
authors.forename: Zhao-hua
authors.initials: ZH
authors.lastname: Zeng
authors.forename: Kevin
authors.initials: K
authors.lastname: Teoh
authors.forename: Arya M
authors.initials: AM
authors.lastname: Sharma
authors.forename: Labib
authors.initials: L
authors.lastname: Abouzahr
authors.forename: Irene
authors.initials: I
authors.lastname: Cybulsky
authors.forename: Andre
authors.initials: A
authors.lastname: Lamy
authors.forename: Lloyd
authors.initials: L
authors.lastname: Semelhago
authors.forename: Robert M K W
authors.initials: RM
authors.lastname: Lee
mesh_terms: D000273:Adipose Tissue / Q000502:physiology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D045462:Endothelium-Dependent Relaxing Factors / Q000032:analysis / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D013895:Thoracic Arteries / Q000737:chemistry / Q000502:physiology*; D014664:Vasodilation
chemical_list: D045462:Endothelium-Dependent Relaxing Factors