Use of Cold Cardioplegic Solution for Vein Graft Distention and Preservation: A Light and Scanning Electron Microscopic Study

To evaluate the effect of a cardioplegic solution on the endothelium of the saphenous vein, portions of this vein were harvested from each of 5 patients undergoing coronary artery bypass operation. Each sample was divided into five segments. One segment was distended with heparinized saline solution, one with heparinized blood, and one with heparinized cardioplegic solution (25 mEq of potassium per liter). All of the distending solutions were kept at 10°C, and pressure was carefully limited to 200 mm Hg. The fourth segment of vein was distended with heparinized saline solution but no effort was made to limit distending pressure, and the fifth segment was not distended. All samples were then examined with light and scanning electron microscopy.There were no great morphological differences in the endothelium of veins distended to 200 mm Hg with saline solution, blood, or cardioplegic solution. The morphology of these samples compared favorably with the control vein endothelium although scattered areas of endothelial disruption were present in every sample. Veins distended without pressure control showed massive endothelial disruption. The particular solution used to distend the saphenous veins is not as important as limiting the distending pressure.     

The influence of harvesting technique on endothelial preservation in saphenous veins.

To study optimal conditions of preparation of saphenous veins as coronary artery bypass grafts, segments of saphenous veins were obtained from 29 consecutive patients undergoing coronary artery bypass grafting. The saphenous vein segments were divided into three groups. In Group I, 10 saphenous vein segments were harvested using a "no-touch" technique without any other preparation aids. In Group II, 10 saphenous vein segments were removed while distended at 70-120 mm Hg with a balanced pH electrolyte solution at 37 degrees C. In Group III, consisting of 10 saphenous vein segments, nitroglycerin (1 microgram/ml) was added to the distending solution used in Group II. Samples of saphenous vein were assessed in a blind study using light and scanning electron microscopy to estimate endothelial cell preservation by the three harvest techniques. Saphenous veins receiving only a no-touch dissection technique without distention solution (Group I) revealed significantly better endothelial preservation (P less than 0.005). The administration of distention solution alone, or with nitroglycerin, to saphenous veins in situ using our operative technique during harvest does not appear to protect endothelial-integrity and may be harmful.     

Atherogenic effect of barotrauma on in situ saphenous veins in monkeys

The objectives of this study were to determine whether veins subjected to barotrauma in situ undergo lipid uptake and morphologic changes to the same extent as veins grafted into the arterial circulation. Saphenous veins in seven stump-tailed macaque monkeys were exposed bilaterally and were circumferentially dissected free from surrounding tissue only at isolated sites. Segments of the veins were distended for 1 minute at hydrostatic pressures of 125 or 350 mm Hg. An undistended segment served as control. A cephalic vein graft was interposed in the femoral artery for comparison with in situ veins. The animals were fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. Saphenous veins and the cephalic vein grafts were explanted at 3 months for biochemical and histologic analyses. Cholesterol content in undistended saphenous veins was similar to that in veins distended at 125 or 350 mm Hg--105 +/- 15, 122 +/- 14, and 109 +/- 30 micrograms/100 mg wet tissue weight, respectively. Cholesterol content in cephalic vein grafts, 473 +/- 122 micrograms/100 mg, was greater (p less than 0.001) than in saphenous veins at all distention pressures studied. There was no difference among the distention pressures in the intimal fraction of saphenous vein wall, with the pooled value being 20% +/- 12%. This contrasted with the value of 59% +/- 11% in cephalic vein grafts (p less than 0.01). Endothelial coverage of the luminal surface in saphenous veins was similar among the levels of barotrauma, with the pooled value being 83% +/- 15%. Less of the lumen was covered with endothelium in cephalic vein grafts, 46% +/- 18% (p less than 0.01). Slightly more medial fibrosis was observed in cephalic vein grafts as compared with saphenous veins (p less than 0.05). These data demonstrate that barotrauma alone does not cause veins that remain in the venous system to undergo the lipid uptake or morphologic changes that occur in veins grafted into the arterial circulation in nonhuman primates.     

Pressure distension stimulates the expression of endothelial adhesion molecules in the human saphenous vein graft

BACKGROUND: Mechanical trauma occurring during saphenous vein graft harvesting plays a major role in graft failure after coronary bypass surgery. There is increasing evidence that neutrophil-endothelial interaction is involved in the pathogenesis of early graft occlusion. This study evaluates the effect of pressure distension on the expression of endothelial adhesion molecules in human saphenous vein. METHODS: Segments of saphenous vein graft (SVG) were collected from 20 patients undergoing coronary bypass surgery. We evaluated the expression of intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and P-selectin on SVG endothelium under basal conditions and after pressure distension at 300 mm Hg. In the same experimental setting we also evaluated adhesion of both unstimulated and activated neutrophils to the endothelium of SVG. RESULTS: Control endothelial cells exhibited only a weak staining for intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and P-selectin, whereas the levels of adhesion molecules increased significantly in the distended veins. Similarly, significantly greater adhesion of both unstimulated and activated neutrophils was observed in distended veins compared with control veins. CONCLUSIONS: Pressure distension of SVG before coronary bypass surgery induces upregulation of endothelial adhesion molecules, with subsequent increase in neutrophil adhesion to the endothelium. Neutrophil adhesion to endothelial cells may contribute to early failure of SVG.     

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.     

Histologic fate and endothelial changes of distended and nondistended vein grafts.

Sixty-two autogenous cephalic vein segments were grafted into the femoral arteries of 31 mongrel dogs, the left side receiving non-distended (control) grafts and the right side distended (experimental) grafts. Distending media were heparinized blood and saline. Veins were distended at 600 mm Hg for 2 minutes. Specimens were taken at intervals from 15 minutes to 3 months, and were studied by gross inspection, surface observations (light scanning stereoscope to X70 scanning electron microscope to X6,000) and routine histologic techniques (light microscope to X 1000). In general, grafting of veins in the arterial system was followed by progressive degenerative changes in all layers of the vein, including endothelial cell involution, desquamation and re-endothelialization. Often a variable degree of subendothelial fibrous and/or myoepithelial proliferation occurred which might compromise even a lumen lined by healthy endothelium. Distention caused these changes to occur earlier (2-4 weeks) and to be more pronounced. Distention with saline caused more damage to the endothelium than did distention with blood. We conclude that preimplant distention of vein grafts (to overcome spasm) should be employed sparingly, as it adversely affects the endothelial covering of the flow surface, accelerates the development of degenerative changes, and may predispose the graft to early thrombotic complications.     

The effect of sodium diatrizoate on the fibrinolytic activity of saphenous vein intima

The objective of this investigation was to assess the effect of 60% sodium diatrizoate on intimal fibrinolytic activity of saphenous vein as it may play an important role in the development of postvenographic thrombophlebitis. Sixteen saphenous vein specimens were obtained from 14 patients during vascular surgical procedures requiring use of the saphenous vein. Immediately after excision, each vein was divided into three segments for study (Groups I, II, and III). Group I specimens were flushed with normal saline and served as controls. Group II specimens were flushed with 60% sodium diatrizoate. Group III specimens were flushed with 60% sodium diatrizoate followed by normal saline 2 min later. Intimal fibrinolytic activity was quantified in each specimen using the modified histochemical method of Todd. The presence of lysis was noted at 10, 20, 30, and 45 min. In Group 1, 5 of the 16 veins demonstrated no baseline intimal fibrinolytic activity and corresponding specimens were not included in the analysis. When comparing Group II to Group I, there was significant delay in intimal fibrinolytic activity with mean appearance times of 36.8 ± 7.8 and 22.3 ± 9.8 min, respectively (P < 0.0005). Likewise, when comparing Group III to Group I, there was significant delay in intimal fibrinolytic activity with times of 37.3 ± 9.3 and 22.3 ± 9.8 min, respectively (P < 0.005). There was no statistical difference between Groups II and III. The fibrinolytic activity of saphenous vein intima is significantly diminished after exposure to sodium diatrizoate. Saline flush does not significantly alter this effect.     

Distention promotes platelet and leukocyte adhesion and reduces short-term patency in pig arteriovenous bypass grafts

A pig model of autologous saphenous vein to common carotid artery bypass grafting was developed. An end-to-end anastomotic technique led to lower middle graft and distal turbulence. Saphenous veins were surgically prepared with or without distention at 600 mm Hg, implanted into the arterial circulation, and removed 2 hours later. Medial integrity was then assessed by adenosine triphosphate/adenosine diphosphate concentration ratio, and endothelial integrity, leukocyte and platelet adhesion by scanning electron microscopy. In grafts made with undistended vein adenosine triphosphate/adenosine diphosphate concentration ratio was not significantly lower (3.0 +/- 0.1, n = 32) than in freshly isolated vein (3.3 +/- 0.1, n = 26), endothelial cover was 98% +/- 1%, n = 6, and there was little platelet or leukocyte adhesion. In distended grafts adenosine triphosphate/adenosine diphosphate concentration ratio was reduced to 2.2 +/- 0.2 (n = 7, p less than 0.005), endothelial cover was reduced to 38% +/- 14% (n = 6, p less than 0.001), and there was extensive platelet and leukocyte adhesion to exposed subendothelium. In separate experiments graft patency measured at 1 to 5 weeks was significantly greater (96%, n = 25) when undistended vein was used than when distended vein was used (64%, n = 25, p less than 0.005). The data show that distention leads to medial and endothelial damage and that this is associated with increased platelet and leukocyte adhesion and with reduced early patency.     

Immunohistochemical and ultrastructural evidence that dendritic cells infiltrate stenotic aortocoronary saphenous vein bypass grafts

We earlier speculated that antigen-presenting dendritic cells may be involved in the immune reactions leading to saphenous vein bypass graft failure. The purpose of this study was to confirm whether dendritic cells are present in stenotic human saphenous vein bypass grafts. Segments of stenotic saphenous vein grafts were explanted from 14 patients at re-do bypass operation and ten normal saphenous veins were harvested during femoro-popliteal grafting. Sections of specimens were analysed using cell type specific antibodies to identify dendritic cells (CD1a, S-100), T-lymphocytes (CD3), macrophages (CD68), smooth muscle cells (alpha-SMA) and endothelial cells (FVIII). Dual immunostaining, confocal immunofluorescent laser scanning microscopy and electron microscopy were used. Stenotic grafts showed structural alterations of intimal hyperplasia and varying degrees of atherosclerotic degeneration. No cells expressing CD1a and S-100 were observed in the intima and media of normal saphenous veins. Cells expressing these antigens were present around areas of medial neovascularization and within intimal atherosclerotic lesions in saphenous vein bypass grafts. Electron microscopy demonstrated the presence of cells containing a well-developed tubulovesicular system which is unique to cells from the dendritic cell family. Double immunohistochemistry and confocal immunofluorescent microscopy revealed the co-localization of T-lymphocytes with dendritic cells. Dendritic cells are present in stenotic saphenous vein bypass grafts. Dendritic cells may be responsible for antigen presentation and modulation of immune reactions in accelerated graft atherosclerosis through their interaction with T-lymphocytes.     

The relative influence of arterial pressure versus intraoperative distention on lipid accumulation in primate vein bypass grafts

Atherosclerotic degeneration has been well documented to be the limiting factor for long-term function of aortacoronary vein bypass grafts. Injury, including that induced by pressure distention in preparation for grafting, is thought to play a role in this degeneration. Injury can be minimized by limiting the distending pressure, but vein grafts are chronically subjected to arterial pressures that far exceed native venous pressure. We evaluated the relative influence of arterial pressure and of higher pressure of distention on cholesterol and apolipoprotein-B accumulation by grafts in our established animal model of graft atherogenesis. Grafts were interposed in the femoral arteries of eight normolipemic stump-tailed macaque monkeys. Before insertion, each vein was distended at 125 mm Hg (arterial pressure) for 1 minute with autologous blood, followed by distention of one half of the vein at 350 mm Hg for 1 additional minute. Grafts and ungrafted control vein were removed 3 months later. Cholesterol concentration in grafts distended at 125 mm Hg was 213% (p less than 0.01) and apolipoprotein-B concentration was 430% (p less than 0.001) of that in ungrafted control veins, whereas in grafts distended at 350 mm Hg cholesterol was 250% (p less than 0.01) and apolipoprotein-B was 925% (p less than 0.001) of the control concentrations. Although morphologic differences between the two groups of grafts were less profound than biochemical differences, foam cells were observed more frequently in grafts distended at 350 mm Hg than in those distended at 125 mm Hg. These data demonstrate that chronic exposure to arterial pressure has a significant effect on graft cholesterol that is proportionally greater than that caused by intraoperative distention at moderate pressure. Nevertheless, the detrimental effects of excessive distending pressures should not be ignored.     

Release of chemotactic factors by veins during preparation for arterial bypass

With the use of arterial bypass release neutrophil chemotactic factors, saphenous veins were removed from dogs by means of standard surgical technique and were distended to a pressure of 200 mm Hg for 15 minutes with cold (4 degrees C) plasmalyte solution. Veins cannulated in situ and flushed with cold (4 degrees C) plasmalyte solution served as negative controls. Experimental and control flush solutions were assayed for the presence of neutrophil chemotactic factors with the use of modified Boyden chambers. Chemotactic activity from the distended vein grafts was 2.2 to 7.2 times the control value. Biologic chemotactic activity was demonstrated as well. These results suggest a role for the vein graft itself in the recruitment of neutrophils to implanted veins by releasing chemoattractants.     

Changes in venous endothelial fibrinolytic activity and histology with in vitro venous distention and arterial implantation

We performed intraoperative pressure monitoring in a clinical setting and demonstrated that the average venous distention pressure observed during preparation of autogenous vein grafts for arterial implantation was 300 to 500 mm Hg and often exceeded 500 mm Hg. Similar data on venous distention pressures were obtained by Ramos et al [4] and by Abbott et al [1]. Although the exact relation between venous distention pressure, venous endothelial fibrinolytic activity and long-term autogenous vein graft patency is unknown, our data suggest that autogenous vein graft distention pressure should be kept under 500 mm Hg during graft procurement and static pressure testing before venous autograft implantation. Ideally, either venous distention pressure should be monitored during vein graft harvesting and preparation, and kept as low as possible, or procured autogenous vein grafts should not be statically distended but rather allowed to gradually enlarge due to pulsatile arterial flow after implantation.     

Human aortocoronary grafts and nitric oxide release: relationship to pulsatile pressure

BACKGROUND: Short and long-term failure of saphenous vein grafts continues to be a significant problem for cardiac surgeons. The purpose of this study was to elucidate the early adaptive changes of human artery and vein conduits with respect to nitric oxide (NO) production under various pressure and pulsatile distention conditions. METHODS: Real-time amperometric NO determinations were made in an in vitro model using human saphenous vein segments (n = 12) and internal thoracic artery segments (n = 8) between 70 and 170 mm Hg, under static conditions recorded with a pressure transducer. Exposing the tissue to morphine (10(-6) M) also stimulated NO release. Under conditions in which the conduits were exposed to the respective pressures for 1 hour, they were then examined for their granulocyte-adhering potential using computer-assisted imaging techniques. RESULTS: A pressure-dependent decrease of NO release was found after 32 minutes of pulsatile pressure (170 mm Hg) in artery and vein, the latter of which appeared to be affected more negatively (p < 0.05; because many more observation points differed significantly after 32 minutes compared to 110 mm Hg values). In vessels maintained for 1 hour at these different pressures and then exposed to morphine (1 microM), stimulated NO release significantly diminished in the veins (artery 37.4 nM NO versus vein 18.1 nM NO; p < 0.05). Increased pressures also correlated with an increase in granulocyte adhesion to veins that could not be reduced following morphine exposure. CONCLUSIONS: Increased pressure and cyclic distention lead to loss of NO release and increased immunocyte adhesion, which are significantly more pronounced in saphenous vein than in internal thoracic artery, suggesting that in the long term this may contribute to the failure of saphenous vein conduits in coronary revascularization.     

A Canine Model of Intimal Hyperplasia (IH) in Autogenous Vein Grafting: A Preliminary Report

High failure rates (10–40% at 1 year and 2–6% per year thereafter) of autologous vein grafts in peripheral bypass surgery due to progressive intimal hyperplasia (IH) have prompted researchers to search for an animal model that develops IH in a relatively short period of time. This study summarizes our experiences in promoting IH in a canine model. Eight to ten centimeters of both jugular veins were exposed in 40 adult mongrel conditioned dogs. After division into 4–5-cm lengths, the segment of jugular vein most proximal was ballooned at 800–900 mm Hg with a modified 8F Fogarty catheter to induce intimal and medial layer injury. The distal segment was left nonballooned. Segments of these autologous vein grafts, 1.5 cm in length, both ballooned and nonballooned, were then anastomosed, end to end, into the carotid and femoral circulations. Six weeks postoperatively the grafts were perfusion-fixed, harvested, and histologically processed, and the amount of the lumen in midgraft sections occupied by IH was determined by image analysis. In all dogs, the degree of IH was significantly greater in the balloon catheterized vs noncatheterized graft segments. IH was more severe in the femoral than in the carotid arteries. The grafts that developed the most severe intimal hyperplasia were femoral grafts that had been balloon catheterized. We conclude that these protocols are effective in inducing IH in a canine model in short postoperative limes.     

Duplex saphenous vein mapping: venous occlusion and dependent position facilitate imaging

The purpose of this study was to develop an optimal technique for greater saphenous vein distention during preoperative duplex assessment. An Acuson 128 scanner with a 7.5-MHz sector probe was used to assess the effects of venous occlusion and dependent position on the diameter of the greater saphenous vein in 20 male volunteers. The greater saphenous vein was imaged 10 cm above and 10 cm below the knee with the subject lying horizontal, horizontal with a thigh tourniquet inflated to 40 mm Hg, inclined at 15 degrees of reversed Trendelenburg, and inclined at 15 degrees of reversed Trendelenburg combined with the tourniquet inflated to 40 mm Hg. Maximal vein diameters and circumferences were measured by a sonographer blinded to the conditions of vein measurement to avoid interpretation bias. Using a t test assuming equal variances, the increases in vein circumferences and diameters achieved by dependency and tourniquet combined were significantly greater than those achieved by dependency alone (p=0.004). The technique of dependency combined with tourniquet inflation to 40 mm Hg facilitates greater saphenous vein imaging and provides an optimal method of venous distention.     

A canine model of intimal hyperplasia (IH) in autogenous vein grafting: a preliminary report

High failure rates (10-40% at 1 year and 2-6% per year thereafter) of autologous vein grafts in peripheral bypass surgery due to progressive intimal hyperplasia (IH) have prompted researchers to search for an animal model that develops IH in a relatively short period of time. This study summarizes our experiences in promoting IH in a canine model. Eight to ten centimeters of both jugular veins were exposed in 40 adult mongrel conditioned dogs. After division into 4-5-cm lengths, the segment of jugular vein most proximal was ballooned at 800-900 mm Hg with a modified 8F Fogarty catheter to induce intimal and medial layer injury. The distal segment was left nonballooned. Segments of these autologous vein grafts, 1.5 cm in length, both ballooned and nonballooned, were then anastomosed, end to end, into the carotid and femoral circulations. Six weeks postoperatively the grafts were perfusion-fixed, harvested, and histologically processed, and the amount of the lumen in midgraft sections occupied by IH was determined by image analysis. In all dogs, the degree of IH was significantly greater in the balloon catheterized vs noncatheterized graft segments. IH was more severe in the femoral than in the carotid arteries. The grafts that developed the most severe intimal hyperplasia were femoral grafts that had been balloon catheterized. We conclude that these protocols are effective in inducing IH in a canine model in short postoperative times.     

Gene delivery to aortocoronary saphenous vein grafts in a large animal model of intimal hyperplasia

OBJECTIVE: More than 50% of aortocoronary saphenous vein grafts are occluded 10 years after surgery. Intimal hyperplasia is an initial, critical step in the progression toward occlusion. To date, no clinically relevant large animal models of aortocoronary saphenous vein graft intimal hyperplasia have been fully characterized. Gene therapy holds promise as a novel treatment for aortocoronary saphenous vein graft intimal hyperplasia. The 2 objectives of this study are to characterize a canine model of aortocoronary saphenous vein graft intimal hyperplasia and to demonstrate that ex vivo gene delivery is possible in these grafts using adenoviral vectors. METHODS: Ten dogs underwent aortocoronary bypass grafting using saphenous veins. Six dogs underwent serial arteriograms to monitor graft patency. On postoperative day 90, the dogs were killed and their grafted and nongrafted saphenous veins were studied histologically. Four dogs underwent the same procedure, but their saphenous veins were treated with 1 x 10(12) total viral particles of a replication-deficient, recombinant adenovirus containing beta-galactosidase (n = 2) or the beta-adrenergic receptor kinase carboxyl terminus (n = 2). These animals were killed on postoperative day 7 for determination of transgene expression. RESULTS: All grafts were demonstrated patent by arteriogram before the animals were killed. The mean intimal area of the saphenous vein grafts was increased when compared with that of the nongrafted saphenous veins (2.83 mm(2) vs 0.09 mm(2), P <.0008). Adenoviral-treated saphenous vein grafts demonstrated positive transgene expression either by X-gal staining (beta-galactosidase) or Northern analysis (beta-adrenergic receptor kinase carboxyl terminus). CONCLUSION: This study characterizes a clinically relevant canine model of aortocoronary saphenous vein graft intimal hyperplasia. In addition, it demonstrates that adenoviral vectors can be delivered ex vivo to the saphenous vein graft vessel wall at subphysiologic distension pressures. This model may be used in future studies to manipulate molecular targets critical in aortocoronary saphenous vein graft intimal hyperplasia.     

Effects of stretch or distention on phenylephrine-induced constriction of human coronary artery bypass grafts

OBJECTIVE: To determine the effects of grafting saphenous veins into the arterial circulation and to compare the responsiveness of saphenous veins and mammary arteries to vasoconstrictors (phenylephrine or potassium) and a vasodilator (the calcium antagonist isradipine). DESIGN: Prospective, controlled, in vitro study. SETTING: Laboratory facility in a university teaching hospital. PARTICIPANTS: Small excess segments of internal mammary arteries or saphenous veins obtained from patients undergoing coronary artery bypass graft surgery. INTERVENTIONS: Vessel segments were cut into rings to measure isometric tension development in isolated tissue chambers. The law of LaPlace for a cylinder was applied to determine tensions in vitro corresponding with arterial or venous tensions in vivo or distending pressures ex vivo. MEASUREMENTS AND MAIN RESULTS: Stretching saphenous vein rings from venous to arterial tensions reduced maximal phenylephrine-induced constriction but did not alter their dose response to phenylephrine, potassium, or isradipine. At arterial tensions, potassium, but not phenylephrine, was more potent in constricting mammary artery than saphenous vein; isradipine was more potent as a vasodilator of potassium-constricted mammary artery than saphenous vein. Maximal phenylephrine-induced or potassium-induced constriction was no different for either vessel at arterial tensions; however, prior distention of veins to tensions corresponding with pressures of 200 or 300 mmHg significantly (p < 0.01, Dunnett's test) reduced subsequent constriction. CONCLUSION: Phenylephrine may be more likely to constrict native internal mammary arteries than distended autogenous saphenous vein grafts in vivo because high-pressure distention of veins markedly inhibits their vasoreactivity.