Traction injury during minimally invasive harvesting of the saphenous vein is associated with impaired endothelial function.

OBJECTIVE: Many methods of minimally invasive surgical harvesting of the great saphenous vein have been developed because of the morbidity related to the long skin incision after traditional (open) great saphenous vein harvesting. One such method involves the use of multiple small incisions separated by 10- to 15-cm skin bridges through which the saphenous vein is harvested. We hypothesized that this method of saphenous vein harvesting might subject the saphenous vein to considerable traction forces, resulting in impaired endothelial cell function. METHODS: Four-millimeter great saphenous vein segments were obtained from patients undergoing elective coronary artery bypass graft surgery. Group A (minimally invasive surgery) consisted of 23 rings from 20 patients (age, 65.8 +/- 11.1 years, mean +/- SD). Group B (open harvesting) consisted of 33 rings from 8 patients (age, 69.8 +/- 8.6 years). All great saphenous vein segments were undistended and were used within 24 hours of harvesting. Isometric tension experiments were performed on each ring of the great saphenous vein by using a force-displacement transducer to measure the force of contraction in grams. Measurements included developed force after exposure to high-potassium depolarizing solution and 50 micromol/L phenylephrine and decrease in force of contraction (relaxation) after exposure to 1 and 10 micromol/L acetylcholine. RESULTS: There were no differences between the minimally invasive surgery and open harvesting groups in their responses to high-potassium depolarizing solution or phenylephrine: high-potassium depolarizing solution, contractions of 4.26 +/- 0.72 g (mean +/- SEM) and 3.95 +/- 0.38 g, respectively (P =.70); phenylephrine, contractions of 3.49 +/- 0.63 g and 2.73 +/- 0.39 g, respectively (P =.41). There was no net relaxation in segments from the minimally invasive surgery group after exposure to 1.0 or 10 micromol/L acetylcholine. In contrast, rings from the open harvesting group demonstrated relaxation of -0.41 +/- 0.07 g and -0.32 +/- 0.09 g after exposure to 1.0 and 10 micromol/L acetylcholine, respectively. CONCLUSIONS: In undistended saphenous vein segments isolated from patients undergoing minimally invasive surgical and open techniques of harvesting, there was no acetylcholine-mediated endothelium-dependent relaxation in the minimally invasive surgery group. Therefore harvesting of the great saphenous vein through multiple small incisions might result in endothelial dysfunction, possibly caused by traction injury.

Effect of moderate pressure distention on the human saphenous vein vasomotor function.

BACKGROUND: Manual pressure distension, which is commonly applied to the human saphenous vein graft for coronary artery bypass, is believed to have detrimental consequences for the graft patency. The vasomotor function of the vein after distention during surgical preparation for grafting and after distention in laboratory conditions at pressure of 50 to 600 mm Hg was studied. The effect of a combination of vasodilative agents to prevent vasospasm was also tested. METHODS: The contractile and dilatory responses of distended and undistended human saphenous veins and those after drug treatment were examined in organ baths under isometric conditions. RESULTS: Distention at the pressure range 100 to 300 mm Hg resulted in an increased contractile response of the saphenous vein to both alpha-adrenergic activation with 50 micromol/L phenylephrine (153.73% +/- 15.69%) and depolarization with 80 mmol/L K(+) (141.03% +/- 15.13%) in comparison with the undistended vein and did not impair the relaxation. In contrast manual distention during surgical preparation abolished the contractile response and impaired the relaxation. The application of a combination of vasodilative drugs (alpha-adrenergic antagonist phenoxybenzamine, 10 micromol/L, Rho-kinase inhibitor HA-1077, 50 micromol/L, and calcium blocker nicardipine, 1 micromol/L) eliminated the contractile response of the vein to phenylephrine and 80 mmol/L K(+). This effect was sustained more than 20 hours after the washout of the drugs. CONCLUSIONS: The distention of the human saphenous vein at moderate pressure combined with the application of the effective combination of vasodilative drugs before grafting into the arterial circulation could be a beneficial alternative to the current practice of uncontrolled pressure distension.

The mechanism of excitation-contraction coupling in phenylephrine-stimulated human saphenous vein.

The human saphenous vein (HSV) is the most widely used graft in coronary artery revascularization procedures and is susceptible to spasm perioperatively. The aim of this study is to elucidate the mechanism(s) of agonist-induced excitation-contraction coupling in this vessel. Isometric contraction experiments were combined with in situ smooth muscle intracellular Ca(2+) concentration ([Ca(2+)](i)) imaging by confocal microscopy of intact undistended HSV segments during activation with phenylephrine (PE; 50 microM). Stimulation with PE produced a sustained contraction. Preincubation with 5 microM nifedipine, a blocker of the L-type voltage-operated Ca(2+) channel, or 50 microM SKF-96365, a blocker of both the voltage- and receptor-operated channels, reduced force generation by 25-30%. Ca(2+) imaging revealed that PE elicited only a transient rise in [Ca(2+)](i), suggesting that Ca(2+) plays only a minor role. However, a requirement for basal Ca(2+) levels was demonstrated when PE contractions could not be maintained in Ca(2+)-free medium. In light of the transient Ca(2+) response, it appears that signals other than Ca(2+) must maintain the tonic contraction elicited by PE, such as those that sensitize the myofilaments to Ca(2+). Application of HA-1077 (a Rho kinase inhibitor) at the peak of the contraction completely abolished the plateau phase of the response, whereas application of genistein (a tyrosine kinase inhibitor) reduced this phase by approximately 50%. The foregoing results suggest that, whereas the transient Ca(2+) signal can contribute to the development of force, maintenance of the plateau phase of the PE contraction in the HSV is the result of myofilament Ca(2+) sensitization by Rho kinase and tyrosine phosphorylation. The elucidation of the mechanisms of excitation-contraction coupling in the HSV may be useful for the development of therapeutic strategies for the alleviation of vein graft spasm.