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J Thorac Cardiovasc Surg 2006;132:1131-1136
© 2006 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Expression of neuronal nitric oxide synthase in the internal thoracic artery and saphenous vein

^a Department of Pharmacology, National University of Singapore, Singapore
^c Department of Medicine, National University of Singapore, Singapore
^d Department of Surgery, National University of Singapore, Singapore
^b Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vt
^e Clinical Trials and Epidemiology Research Unit, Singapore

Received for publication February 8, 2006; revisions received July 24, 2006; accepted for publication August 3, 2006.

^_* Address for reprints: George D. Webb, PhD, Department of Molecular Physiology and Biophysics, University of Vermont, College of Medicine, HSRF Building, Burlington, VT 05405 (Email: webb{at}physiology.med.uvm.edu).

OBJECTIVES: Endothelial nitric oxide synthase (type III) generates nitric oxide, which dilates blood vessels. Recently, it was discovered that arterial smooth muscle cells express neuronal nitric oxide synthase (type I). The purpose of this study was to determine the relative amounts of neuronal nitric oxide synthase in the human internal thoracic artery and saphenous vein.

METHODS: Remainder segments of internal thoracic arteries and saphenous veins were obtained from 45 patients during coronary artery bypass grafting. Western blotting used specific antibodies against the 3 isoforms of human nitric oxide synthase and ß-actin (for normalization) to measure the relative amounts of the 3 isoforms of nitric oxide synthase proteins in vessel specimens. Immunohistochemistry was used to localize the 3 proteins in specific cells.

RESULTS: Western blotting detected all 3 isoforms of nitric oxide synthase in the human internal thoracic artery. The band density (normalized to ß-actin) of neuronal nitric oxide synthase was not significantly different from the band density of endothelial nitric oxide synthase. The amounts of neuronal nitric oxide synthase in arteries and veins were equal. Immunohistochemistry showed that the highest expression of endothelial nitric oxide synthase was in endothelial cells, but some expression was also seen in smooth muscle cells. Most of the neuronal nitric oxide synthase was in smooth muscle cells. The location and relative amounts of inducible nitric oxide synthase were variable.

CONCLUSIONS: Neuronal nitric oxide synthase is expressed in the vascular smooth muscle of patients undergoing bypass, and the amount in the internal thoracic artery is the same as in the saphenous vein.

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