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J Thorac Cardiovasc Surg 2005;130:1130-1136
© 2005 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Perivascular adipose tissue modulates vascular function in the human internal thoracic artery

^a Department of Anaesthesia, McMaster University, Hamilton, Ontario, Canada
^b Department of Cardiovascular Surgery, McMaster University, Hamilton, Ontario, Canada
^c Department of Medicine, McMaster University, Hamilton, Ontario, Canada

Received for publication April 7, 2005; revisions received May 10, 2005; accepted for publication May 25, 2005.

^_* Address for reprints: Yu-Jing Gao, MD, PhD, Department of Anaesthesia, McMaster University, 1200 Main St West, Hamilton, Ontario, Canada L8N 3Z5 (Email: gaoyu{at}mcmaster.ca).

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 µmol/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 µmol/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.

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