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Eur J Cardiothorac Surg 2000;17:175-181
© 2000 Elsevier Science NL
a Division of Surgery/Cardiac Surgery, Innsbruck University Hospital, University of Innsbruck, Innsbruck, Austria
b Institute for Medical Chemistry and Biochemistry, University of Innsbruck, Innsbruck, Austria
Corresponding author. Tel.: +43-512-504-3806/2529; fax: +43-512-504-2528
e-mail: johannes.o.bonatti{at}uibk.ac.at
Objective: It has been shown previously that the internal mammary artery releases more cyclic guanosine monophosphate after stimulation with atrial natriuretic peptide than the saphenous vein, and that C-type natriuretic peptide possesses a cyclic guanosine monophosphate stimulating potential on saphenous vein bypass grafts. The present study was undertaken to investigate intracellular content and extracellular release of cyclic guanosine monophosphate, by the internal mammary artery and saphenous vein, after challenge with further members of the natriuretic peptide family. Methods: Specimens of human internal mammary artery and saphenous vein from 29 patients were cut into segments and stimulated with 10-6 M concentrations of atrial natriuretic peptide (internal mammary artery n=8, saphenous vein n=10), brain natriuretic peptide (internal mammary artery n=9, saphenous vein n=13), C-type natriuretic peptide (internal mammary artery n=12, saphenous vein n=15), and urodilatin (internal mammary artery n=8, saphenous vein n=12). Intracellular content and extracellular release of cyclic guanosine monophosphate were determined using an 125I radioimmunoassay. Results: The following median stimulated intracellular cyclic guanosine monophosphate concentrations were measured in the internal mammary artery and saphenous vein: 35358 and 8672 fmol/cm2 (P<0.001) after atrial natriuretic peptide, 45632 and 7830 fmol/cm2 (P=0.003) after brain natriuretic peptide, 10144 and 13216 fmol/cm2 (P=NS for intergraft comparison) after C-type natriuretic peptide, and 20949 and 6690 fmol/cm2 (P=0.001) after urodilatin. Stimulation with atrial natriuretic peptide, brain natriuretic peptide and urodilation also led to a significant increase of extracellular cyclic guanosine monophosphate release by the internal mammary artery. Conclusion: We conclude that brain natriuretic peptide and urodilatin exhibit a similarly effective cyclic guanosine monophosphate-stimulating potential on the internal mammary artery as atrial natriuretic peptide. In contrast, C-type natriuretic peptide shows comparable effects on the internal mammary artery and saphenous vein.
Key Words: Coronary artery bypass Internal mammary artery Saphenous vein Natriuretic peptides
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