It is well established that spasm of an arterial and venous graft conduit may occur during harvesting or after coronary artery bypass grafting (CABG). The antivasoconstrictor effect of levcromakalim and rilmakalim, K(+) channel openers (KCOs), was studied in isolated human internal mammary artery (HIMA) and human saphenous vein (HSV) prepared for CABG. HIMA and HSV rings were contracted by electrical field stimulation (EFS, 20 Hz ) or with exogenous noradrenaline (NA). Levcromakalim induced a concentration-dependent and equipotent inhibition of contraction of HIMA and HSV preconstricted by EFS and exogenoulsy applied NA, while rilmakalim produced a stronger inhibition of EFS- than NA-evoked contractions. Glibenclamide, a selective ATP-sensitive K(+) channel (K(ATP) channel) blocker, significantly antagonized levcromakalim-induced inhibition of EFS- and NA-evoked contractions, as well as rilmakalim-induced inhibiton of EFS-evoked contractions on HIMA and HSV. However, glibenclamide failed to antagonize rilmakalim-induced inhibition of NA-evoked contractions. The results suggest that the antivasoconstrictor effect of levcromakalim occurs postsynapticaly by the opening K(ATP) channels in the vascular smooth muscle cells. They also suggest that the effect of rilmakalim on EFS-evoked contractions involves K(ATP) channels located pre-synaptically. However, the mechanism by which rilmakalim inhibits NA-evoked contraction seems to be K(ATP) channel independent and warrants further elucidation.

The present study was undertaken to examine the effects of pinacidil and levcromakalim, two potassium, channel openers, on human internal mammary artery (HIMA) obtained from patients undergoing coronary artery bypass surgery, and to clarify the contribution of different K+ channel subtypes in pinacidil and levcromakalim action in this blood vessel. Pinacidil and levcromakalim induced a concentration-dependent relaxation of the precontracted arterial segments (pEC50 = 5.77 +/- 0.05 and 6.89 +/- 0.03, respectively), 4-Aminopyridine (3 mM), a non-selective blocker of K+ channels, induced significant shifts to the right of the concentration-response curves for pinacidil and levcromakalim. Tetraethylammonium (6 mM), charybdotoxin (0.4 microM) and apamin (0.1 microM), blockers of Ca(2+)-sensitive K+ channels, had no effect on the pinacidil- and levcromakalim-evoked relaxation. Glibenclamide (0.1-10 microM), a selective blocker of adenosine triphosphate (ATP)-sensitive K+ channels, competitively antagonized the response to levcromakalim (pKB = 7.92 +/- 0.07). In contrast, glibenclamide, in significantly higher concentrations (3-30 microM), non-competitively antagonized the response to pinacidil. High concentrations of pinacidil (> 10 microM) relaxed arterial rings bathed by a medium containing 100 mM K+ with maximum response 83 +/- 6%. Under the same conditions, the maximum levcromakalim-induced relaxation on HIMA was almost abolished (15 +/- 2%). It is concluded that pinacidil and levcromakalim do not relax the HIMA through the same subtype of K+ channel. ATP-sensitive K+ channels are probably involved in levcromakalim- but not in a pinacidil-induced relaxation in the HIMA. In addition, in pinacidil-induced relaxation of the HIMA, K+ channel-independent mechanisms seem to be involved.

PTA with or without stenting was relatively simple, efficient and safe procedure. It required short hospitalization with low treatment costs. If any of suboptimal results or chronic occlusions were present, the implantation of endovascular stents should have been considered.

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