The future of coronary artery bypass grafting (CABG) lies in the greater use of arterial conduits to increase the duration of clinical benefits (González-Santos et al., Rev Esp Cardiol 58:1207, 2005). In the present study, we used porcine arteries given they are a well-established animal experimental model in cardiac surgery and to avoid the influence of the main cardiovascular risk factors of patients undergoing CABG. The aim of this work was to determine functional differences in neurogenic contractions between the isolated internal mammary artery (IMA) and radial artery (RA). Arterial rings were mounted in organ baths for isometric force recordings.

Electrical field stimulation (EFS) evoked frequency-dependent, tetrodotoxin-sensitive contractions in IMA and RA. This neurogenic contraction was markedly inhibited by guanethidine (10-5M) and phentolamine (10-5M). In denuded rings, NO synthase inhibition (L-NOArg; 10-4M) increased contractile responses at the lowest frequencies in the IMA, but did not effect RA contraction. A cyclooxygenase inhibitor (indomethacin; 3x10-6M) reduced neurogenic contractions in IMA while RA contractions were unaltered. The Ca²⁺-activated K⁺ channel blocker, tetraethylammonium (10-3M), enhanced contractions induced by EFS in both segments. However, the voltage-dependent K⁺ channel blocker, 4-aminopyridine (10-4M), increased the neurogenic contraction only in the IMA. In both preparations, neurogenic contraction was unaffected by an ATP-sensitive K⁺ channel blocker, glibenclamide (10-6M), and a radical scavenger, superoxide dismutase (150 U/ml). Our results indicate differences in the mechanisms involved in adrenergic contraction in the two arterial conduits.

This study was supported by grant nordm; PI031257 from FIS.