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J Thorac Cardiovasc Surg 1996;112:264-272
© 1996 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

TISSUE CONCENTRATIONS OF ENDOTHELINS AND FUNCTIONAL EFFECTS OF ENDOTHELIN-RECEPTOR ACTIVATION IN HUMAN ARTERIES AND VEINS

Supported by grants from the Swedish Medical Research Council, the Heart and Lung Foundation, the Wiberg Foundation, the Wallenberg Foundation, the Thuring Foundation, the Swedish Society for Medicine, the Salus Foundation, and funds from the Karolinska Institute.

Received for publication July 20, 1995 Revisions requested Oct. 9, 1995; revisions received Nov. 17, 1995 Accepted for publication Jan. 3, 1996. Address for reprints: Anders Franco-Cereceda, MD, PhD, Department of Thoracic Surgery, Karolinska Hospital, 171 76 Stockholm, Sweden.

Abstract

In the present study, the tissue content and functional effects of endothelin-1 and endothelin-3 were examined in human vessels of importance in coronary bypass operations. Human coronary arteries (i.e., the left anterior descending coronary artery) were obtained from eight cardiac valve donors within 6 hours after death, pulmonary arteries were perioperatively obtained from 15 patients operated on because of lung tumors, and internal thoracic arteries and great saphenous and cephalic veins were obtained at coronary bypass operations from a total of 28 patients. Endothelin-1 and endothelin-3 content was quantified by radioimmunoassay. For functional experiments, the vessels were mounted in organ baths for recordings of isometric contractions in response to endothelin-1, endothelin-3, and the endothelin_A- receptor agonist sarafotoxin 6c. In all vessels investigated, the endothelin-1 content was higher than that of endothelin-3. The highest levels were found in the left anterior descending coronary artery, followed in declining order by the internal thoracic artery, pulmonary artery, saphenous vein, and cephalic vein. Endothelin-1 contracted all vessels in a concentration-dependent fashion. This effect was enhanced in the left anterior descending and internal thoracic arteries by inhibition of nitric oxide and prostaglandin formation. The contractile effect was attenuated in a concentration-dependent fashion in all vessels by incubation with the endothelin_A-receptor blocker BQ-123. Furthermore, contractions evoked by endothelin-1 in the left anterior descending coronary and pulmonary arteries were antagonized by the combined endothelin_A- and endothelin_B-receptor blocker bosentan. Endothelin-3 contracted the left anterior descending coronary and pulmonary arteries and the saphenous vein, but not the internal thoracic artery, in a BQ-123–sensitive fashion. However, after inhibition with nitric oxide or prostaglandin, endothelin-3 also contracted the internal thoracic artery, and the response in the left anterior descending coronary artery was enhanced. Sarafotoxin 6c evoked a BQ-123–sensitive contraction of the left anterior descending coronary artery. It is concluded that endothelin_Areceptors mediate the major portion of the vasoconstriction observed on exposure to endothelin-1, endothelin-3, and sarafotoxin 6c in the left anterior descending coronary, pulmonary, and internal thoracic arteries and the saphenous vein. Furthermore, endothelin_B-receptor activation, with subsequent formation of nitric oxide or prostaglandin (or both), counteracts the vasoconstrictor response to endothelin in the left anterior descending coronary and internal thoracic arteries, but not in the pulmonary artery or saphenous vein. The present findings therefore suggest that endothelin_A-receptor antagonism might prove beneficial in preventing possible endothelin-induced coronary graft spasm. (J THORAC CARDIOVASC SURG 1996;112:264-72)

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