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Ann Thorac Surg 2006;81:1715-1719
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

Potassium Channel-Related Relaxation by Levosimendan in the Human Internal Mammary Artery

Oguzhan Yildiz, MD, PhD a , b , c , * , Melik Seyrek, MD a , b , c , Vedat Yildirim, MD a , b , c , Ufuk Demirkilic, MD a , b , c , Cahit Nacitarhan, MD, PhD a , b , c

a Department of Pharmacology, Gulhane School of Medicine, Ankara, Turkey
b Department of Cardiovascular Surgery, Gulhane School of Medicine, Ankara, Turkey
c Department of Pharmacology, Faculty of Medicine, Akdeniz University, Antalya, Turkey

Accepted for publication December 8, 2005.

* Address correspondence to Dr Yildiz, Gulhane School of Medicine, Department of Pharmacology, Etlik, 06018, Ankara, Turkey (Email: oyildiz{at}gata.edu.tr).

BACKGROUND: Levosimendan is a potent inotropic and vasodilator drug used in the treatment of decompensated heart failure. There is no study on in vitro effects of levosimendan in human isolated arteries.

METHODS: We investigated the effect of levosimendan on contractile tone of human isolated internal mammary artery (IMA). The responses in IMA were recorded isometrically by a force-displacement transducer in isolated organ baths. Levosimendan was added to organ baths either at rest or after precontraction with phenylephrine (1 µmol/L). Levosimendan-induced relaxations were tested in the presence of cyclooxygenase inhibitor indomethacin (10 µmol/L), nitric oxide synthase inhibitor N 122-nitro-L-arginine methyl ester (100 µmol/L), large-conductance calcium-activated potassium-channel inhibitor tetraethylammonium (1 mmol/L), adenosine triphosphate–sensitive potassium-channel inhibitor glibenclamide (10 µmol/L), and voltage-sensitive potassium-channel inhibitor 4-aminopyridine (1 mmol/L).

RESULTS: Levosimendan (10 nmol/L to 3 µmol/L) produced potent relaxation in human IMA (maximal effect, 75.3% ± 4.9% of phenylephrine maximum contraction, 6.8 ± 0.1, n = 15; –log10 of 50% effective concentration). Vehicle had no significant relaxant effect. The relaxation to levosimendan is not affected by either potassium-channel inhibitors (tetraethylammonium and 4-aminopyridine) or cyclooxygenase and nitric oxide synthase inhibitors. Glibenclamide (10 µmol/L) inhibited levosimendan-induced relaxation significantly (p < 0.01).

CONCLUSIONS: Levosimendan effectively and directly decreases the tone of IMA. The mechanism of levosimendan-induced relaxation in IMA appears in part to be adenosine triphosphate–sensitive potassium-channel opening action. Levosimendan may be a cardiovascular protective agent by its relaxing action on the major arterial graft, IMA.






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