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J Thorac Cardiovasc Surg 1995;110:1005-1012
© 1995 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

REACTIVITY OF HUMAN SAPHENOUS VEINS AT ARTERIAL PERFUSION PRESSURES

Nancy J. Rusch, PhDa,b, Theresa A. Wooldridge, BAa, Clark C. Kulig, BAc, G. Hossein Almassi, MDb, Alfred C. Nicolosi, MDb, Gordon N. Olinger, MDb, Lawrence E. Boerboom, PhDb


Milwaukee, Wis.

Supported by grants NIH HL-29587 (N. J. R.) and HL-41840 (L. E. B.) and an award from the Max Baer Heart Fund of the Fraternal Order of Eagles.

Received for publication Dec. 19, 1994. Accepted for publication March 24, 1995. Address for reprints: Nancy J. Rusch, PhD, Associate Professor of Physiology, Human Vascular Biology Laboratory, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226.

Abstract

Vasospasm of human saphenous vein grafts has been reported after aorta-coronary bypass operations. However, it is unknown whether venoarterial grafts are inherently responsive to vasoconstrictor stimuli after implantation into the arterial circulation or whether their vasomotion is secondary to hemodynamic changes. Thus in this study we used in vitro methods to directly evaluate whether isolated human saphenous vein segments respond to vasoconstrictor agents at arterial pressure levels. External diameter and intraluminal flow were monitored in 12 human saphenous vein segments, which were perfused at 30 ml/min with physiologic salt solution at 90, 70, and 50 mm Hg. Increasing intraluminal pressure higher than 50 mm Hg or exposing the vein to Ca2+ -free media did not increase vessel external diameter or intraluminal flow, which suggests that human saphenous veins were fully distended at pressures of 50 mm Hg or greater. However, all human saphenous veins were activated by a 1µmol/L dose of norepinephrine at 50 mm Hg and dilated during subsequent intraluminal infusion of a 1µmol/L dose of acetylcholine, showing intact vascular smooth muscle and endothelial cell function. In the same vessels, a 1µmol/L concentration of 5-hydroxytryptamine constricted human saphenous veins by 19%, 22%, and 26% at intraluminal pressures of 90, 70, and 50 mm Hg, respectively, and reduced vessel flow by 6%, 24%, and 42% at the same pressure levels. Similarly, a 1µmol/L concentration of norepinephrine constricted vessels pressurized at 90, 70, and 50 mm Hg by 9%, 12%, and 17%, respectively, and attenuated vessel flow by as much as 32%. We conclude that human saphenous vein segments are fully distended at perfusion pressures greater than 50 mm Hg, but can dynamically constrict to vasoactive agonists and regulate graft flow at intraluminal pressures as high as 90 mm Hg. Our findings in isolated human saphenous vein segments lend support to clinical observations that human saphenous vein grafts should be regarded as vasoactive conduits after implantation at arterial pressure levels. (J THORAC CARDIOVASC SURG 1995;110:1005-12)

Although aorta-coronary surgery with saphenous vein bypass grafting is an established procedure, surprisingly little is known about the contractile behavior of human saphenous vein (HSV) grafts at arterial pressures. HSV grafts are commonly depicted as inert conduits incapable of vasomotion. Go Go 1-3 However, a growing number of clinical reports suggest that vasospasm of implanted HSV provokes angina, hypotension, and ventricular fibrillation in patients after aorta-coronary bypass operations Go Go 4-6 and also occurs inpatients after long-term implantation of these grafts. Go Go 7-13 Furthermore, vasospasm of HSV grafts may contribute to early graft closure, perhaps as a result of disruption of the endothelial cell layer during severe vessel constriction. Go 5 This may compound the endothelial trauma induced by surgical procedures during graft preparation. Go Go 14-16 Because spasm of HSV grafts has been implicated in the postoperative morbidity of aorta-coronary bypass operations, it is important to evaluate the vasoconstrictor capabilities of these vessels to putative spasmogens at arterial pressure levels.

In this regard, earlier investigators have used angiographic methods to assess the vasoactivity of permanently implanted HSV grafts. Go Go Go 1,17-19 Several studies suggest that the diameters of implanted grafts are insensitive to the dilating effects of tachycardia and local infusion of nitrates, implying that they are fully distended at arterial blood pressure levels and lack intrinsic vasomotor tone. Go Go Go 17,18,20 Nevertheless, Hanet, Robert, and Wijns Go 20 recently reported that although implanted HSV grafts were devoid of inherent vasomotor tone, they constricted strongly to infusion of ergonovine, suggesting that these vessels actively regulate their diameter after implantation into the arterial circulation. Go 18 However, evaluating the direct effect of vasoconstrictor drugs on implanted graft reactivity is difficult, because the inherent reactivity responses of the graft may be masked by concurrent changes in hemodynamic variables. Go Go 1,19 An alternative approach is to use in vitro perfusion methods to directly record the vasoreactivity of isolated, cannulated segments of HSV. In the current study, we used this method to assess whether diameter and intraluminal flow of HSV segments are regulated by vasoconstrictor stimuli at arterial pressure levels.

METHODS

Vein preparations
Distal segments of HSV from aorta-coronary bypass operations were obtained immediately after vein removal and before procedures for graft preparation. The vessel segments were transported to the laboratory in cold Plasma-Lyte solution (Baxter Healthcare Corp., Deerfield, Ill.) and handled according to the standards of the institutional pathogen committee. Vein segments were classified as surgical specimens and were exempted by the institutional human review board from patient consent requirements. Vessel segments were from 12 male patients (11 white, 1 black) with an average age of 66 ± 3 years (range 49 to 73 years). All veins were briefly cleaned of loose adventitial tissue with care taken to preserve vascular endothelium and smooth muscle cell layers.

In vitro vessel perfusion
Vein segments (length 2.5 to 3 cm) were placed in a vascular perfusion chamber (volume 25 ml) and superfused with a physiologic salt solution (PSS) at 5 ml/min by a small peristaltic pump. The vessel ends were mounted on opposing cannulas for intraluminal perfusion and pressurization (Fig. 1). Because the in situ length of the vein segments was unknown, vessel length was adjusted by separating the mounting cannulas until the vessel was linearly extended and showed no lateral bowing during pressurization. Side branches were secured with 5-0 silk ties and the vein was pressurized to 50 mm Hg and independently perfused with PSS at 30 ml/min from a reservoir. External diameter (De) was monitored by a continuous on-line video technique described in detail elsewhere, Go 21 and data were acquired by CODAS software (Dataq Instruments, Akron, Ohio) and stored on a computer for analysis. Although this imaging technique also permits resolution of internal diameter in small vessels, the thick wall of the HSV precluded visualization of internal dimensions in this study.



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  		Fig. 1. Apparatus used to measure De and intraluminal flow in pressurized, perfused HSV segments.

 
Veins were perfused at nonoscillating pressures, and mean intraluminal flow was monitored by collection of the outflow perfusate in a calibrated cylinder. Although the nonoscillating flow pattern used in this study differs from the pulsatile flow pattern found in vivo, pressure-flow curves are reportedly similar between HSV segments perfused by pulsatile and nonpulsatile pressure patterns. Go 3 Flow was adjusted by regulating an outflow resistor distal to the vessel. Inflow and outflow pressures were measured continuously by pressure transducers and were regulated by adjusting the height of the reservoir containing the PSS perfusate. In drug-free PSS, inflow and outflow pressures were the same, suggesting that the cannula tips and vein diameter did not offer significant resistance to perfusate flow. The PSS perfusate and superfusate were composed of (in millimoles per liter) NaCl 119, KCl 4.7, MgSO4 1.17, CaCl2 1.6, NaH2PO4 1.18, NaHCO3 24, ethylenediaminetetraacetic acid 0.026, and glucose 5.5. PSS was maintained at 37° C and aerated with a gas mixture composed of 15% O2, 7% CO2, and 78% N2 to maintain pH at 7.4 in the perfusion and reservoir chambers.

Measurements of graft reactivity
After the vessels were mounted, segments were perfused at 30 ml/min for 1 hour to permit equilibration at an intraluminal pressure of 50 mm Hg and to allow time for drug washout. Vascular reactivity was assessed in all vessels (n = 12) by verifying the ability of the vein to contract to superfusion with norepinephrine, 1 µmol/L. Endothelial function also was verified in each segment by demonstrating that norepinephrine-contracted vessels dilated in response to intraluminal perfusion of acetylcholine, 1 µmol/L. Vessels were then perfused (30 ml/min) and superfused with drug-free PSS to reestablish basal De and flow values for 30 minutes. In 6 of the 12 HSV segments, we tested for the presence of inherent vasomotor tone by comparing De and flow changes (1) in vessels pressurized at 50 mm Hg and perfused and superfused with PSS to establish baseline values, (2) in vessels pressurized at 90 mm Hg and perfused and superfused with PSS, and (3) in vessels pressurized at 90 mm Hg and perfused and superfused with a Ca2+ free PSS to abolishactive tone. The composition of the Ca2+ -free PSS was (in millimoles per liter) NaCl 92, KCl 4.7, MgSO4 1.2, MgCl2 20, NaHCO3 24, NaH2PO4 1.18, ethylenediaminetetraacetic acid 0.026, and glucose 5.5. Go 22

Reactivity to vasoconstrictor agonists
In the remaining six veins in which smooth muscle and endothelial function were evaluated, we examined whether vessels were responsive to norepinephrine and 5-hydroxytryptamine (5-HT) at arterial pressure levels. HSV segments were equilibrated at an intraluminal pressure of 90 mm Hg, perfused with PSS at 30 ml/min, and superfused with drug-free PSS. Vessel De and flow changes induced by superfusion with a 1 µmol/L dose of norepinephrine or a 1 µmol/L dose of 5-HT were measured at 90 mm Hg and then during stepwise pressure reductions from 90 mm Hg to 70 and 50 mm Hg in the continued presence of the vasoconstrictor drug.

Drugs
Norepinephrine, 5-HT, and acetylcholine were obtained from Sigma Chemical Company (St. Louis, Mo.). All drugs were prepared as 1 mmol/L aqueous stock solutions, which were added by aliquot directly to the perfusate or superfusate PSS to obtain the final drug concentrations.

Statistics
Data are expressed as mean plus or minus the standard error of the mean. Statistical comparisons were done by analysis of variance with repeated measures. Significant differences between specific means were determined by Duncan's new multiple range test. A value of p < 0.05 was considered significant.

RESULTS

Graft viability and vasomotor tone
Fig. 2, A, shows an on-line recording of De from an isolated HSV superfused with norepinephrine, 1 µmol/L, and subsequently perfused with acetylcholine, 1 µmol/L, to test for endothelium-dependent relaxation. At an intraluminal pressure of 50 mm Hg, average resting De was 3.54 ± 0.14 mm in 12 veins. In the same vessels, superfusion with a 1 µmol/L concentration of norepinephrine reduced control De by 17% to 2.93 ± 0.16 mm, which verified the presence of contractile vascular smooth muscle cells. Subsequent intraluminal perfusion with acetylcholine, 1 µmol/L, dilated vessels by 38% (n = 12), which indicated viability of the endothelial cell layer. In a subset of six vessels, we tested whether isolated HSVs showed resting vasomotor tone in the arterial pressure range between 50 and 90 mm Hg. Fig. 2, B, shows that vein De measured in vessels perfused at 30 ml/min and maintained at an intraluminal pressure of 50 mm Hg averaged 3.58 ± 0.22 mm. When intraluminal pressure was increased to 90 mm Hg by elevation of the perfusion reservoir for 30 minutes, graft De and flow were unchanged. Similarly, vessel De and flow also were unaffected by 30 minutes of vessel perfusion and superfusion with Ca2 -free PSS to abolish active vascular tone, which indicated that HSVs were fully distended and devoid of resting vasomotor tone at pressures of 50 mm Hg or greater.




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  		Fig. 2. A, Effects of norepinephrine (NE) and acetylcholine (ACH) on diameter (De) of HSV pressurized at 50 mm Hg and perfused at 30 ml/min. Original tracing shows that superfusion with a 1 µmol/L doseof norepinephrine reduced De from 3.68 mm to 2.52 mm, whereas intraluminal perfusion of a 1 µmol/L dose of acetylcholine partially reversed this constriction. B, Bar graph showing mean diameter of six HSV perfused and superfused (1) with PSS at 50 mmHg, (2) with PSS at 90 mm Hg, and (3) with Ca2+-free PSS at 90 mm Hg. Diameter was not increased by increasing pressure or byCa2+-free PSS, implying that veins were already fully distended at 50 mm Hg.

 
Reactivity to vasoconstrictor agonists
We assessed the vasoconstrictor effects of norepinephrine and 5-HT on vessel De and flow at 90 mm Hg and then during stepwise, acute decreases in intraluminal pressure from 90 mm Hg to 70 and 50 mm Hg. Continuous recordings of De in two different HSV segments are shown in Fig. 3. Veins that were initially equilibrated at 90 mm Hg and perfused (30 ml/min) and superfused with drug-free PSS for 30 minutes showed an average De control value of 3.59 ± 0.17 mm. Superfusion with norepinephrine (Fig. 3, left traces) or with 5-HT (Fig. 3, right traces), both in concentrations of 1 µmol/L, actively constricted all vessels pressurized at 90 mm Hg. Some HSV segments were only moderately responsive to vasoconstrictors at 90 mm Hg (vein 1), whereas other vessels showed intense constrictor responses at this pressure (vein 2). When perfusion pressure was acutely lowered from 90 mm Hg to levels of 70 and 50 mm Hg, the constrictions to norepinephrine and 5-HT were enhanced (Fig. 3). Fig. 4, A, shows that compared with results in HSV segments perfused at 90 mm Hg in PSS (control veins), superfusion with a 1 µmol/L dose of norepinephrine significantly reduced vein De at 90, 70, and 50 mm Hg by 9% ± 2%, 12% ± 3%, and 17% ± 3%, respectively (n = 6). In the same vessels, norepinephrine did not significantly reduce flow at 90 mm Hg, but it markedly decreased flow by 13% ± 4% and by 32% ±3% at 70 and 50 mm Hg, respectively (Fig. 4, B). 5-HT was a more potent vasoconstrictor than norepinephrine, as shown by the bar graphs in Fig. 5, A and B (n = 6). This agonist attenuated De and flow in HSV segments perfused at 90 mm Hg by 19% ± 6% and 6% ± 1%, respectively, and these responses were potentiated when pressure was lowered to 70 and 50 mm Hg. The averaged data show that 5-HT attenuated vessel De and flow by 23% ± 7% and 24% ± 7%, respectively, at 70 mm Hg and by 26% ± 7% and 42% ± 6%, respectively, at 50 mm Hg. Norepinephrine-induced responses averaged about 40% less in the same veins at the lower pressures. Stepwise lowering of intraluminal pressure during norepinephrine and 5-HT exposure also induced a fall in outflow (but not inflow) pressure in five of six veins, which suggests that venous contraction to agonists was partially occluding internal vessel diameter.




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  		Fig. 3. Original traces showing effects of norepinephrine (NE) and 5-HT on diameter (De) of two different HSV segments (vein 1, top traces; vein 2, lower traces). Veins initially were perfused with PSS at 30 ml/min at 90 mm Hg and then superfused with either norepinephrine (left traces) or 5-HT (right traces). During drug superfusion, intraluminal pressure was decreased from 90 mm Hg to 70 and 50 mm Hg.

 



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  		Fig. 4. Effect of a 1 µmol/L dose of norepinephrine (NE) on diameter (De) and intraluminal flow of six HSVs at 90 mm Hg and during stepwise pressure changes to 70 and 50mm Hg. A, Bar graph of mean De. B, Bar graph of flow changes to norepinephrine. Open bars (control) represent values in veins perfused with PSS at 30 ml/min at 90 mm Hg and superfused with drug-free PSS. Filled bars signify responses to a 1 µmol/L dose of norepinephrine as percent of control. Asterisk indicates significant difference from control value. Control diameter and flow at 90 mm Hg in drug-free PSS were 3.59 ± 0.17 mm and 30 ml/min, respectively.

 



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  		Fig. 5. Effect of a 1 µmol/L dose of 5-HT on diameter (De) and intraluminal flow of six HSVs at 90 mm Hg and during stepwise pressure changes to 70 and 50 mm Hg. A, Bar graph of mean De. B, Bar graph of flow changes to 5-HT. Open bars (control) represent values in veins perfused with PSS at 30 ml/min at 90 mm Hg and superfused with drug-free PSS. Filled bars signify responses to a 1 µmol/L dose of 5-HT as percent of control value. Asterisk indicates significant difference from control value. Plus sign indicates significant difference from same measurement in norepinephrine superfusate (Fig. 4, A and B). Control diameter and flow at 90 mm Hg in drug-free PSS were 3.59 ± 0.20 mm and 30 ml/min, respectively.

 
DISCUSSION

The main goal of this study was to determine whether isolated HSV segments actively respond to vasoconstrictor stimuli at arterial perfusion pressures. In this respect, our findings provide the first evidence that HSVs are inherently vasoactive conduits at arterial pressure levels that can dynamically regulate their flow in response to endogenous vasoconstrictor substances. Our study also confirms the findings of Dobrin and colleagues, Go 3 who reported that HSV segments lack resting vasomotor tone and behave as rigid tubes at intraluminal pressures higher than 50 mm Hg. Chronically implanted HSV grafts also reportedly lack inherent vasomotor tone, Go Go Go 17,18,20 but our findings in fresh HSVs may not be applicable to long-term grafts that show altered responsiveness to contractile agonists after implantation. Go Go 23-26 It alsoshould be acknowledged that our values for De are not quantitatively coupled to flow alterations, because flow through a conduit is an inverse function of the fourth power of the internal radius, and we were limited to imaging external vein dimensions in this study. In addition, Poiseuille's law states that flow is inversely proportional to conduit length, and thus for the same levels of constriction, flow through our HSV segments likely decreased less than would be expected for longer aorta-coronary vein conduits.

Vasoconstrictor sensitivity
Our findings that HSVs actively contract to vasoconstrictor agonists at intraluminal pressures as high as 90 mm Hg contrast with those of Dobrin and colleagues, Go 3 who evaluated the biomechanical properties of HSV segments in a cannulated vessel preparation. In their report, HSV pressurized at 100 mm Hg showed only a 3% constriction in response to supramaximal doses of norepinephrine, Go 3 whereas at the slightly lower pressure of 90 mm Hg we observed a 17% constriction to a lower norepinephrine concentration. The reason for this difference is not readily apparent, but may relate to different vessel sizes or to differing methods of vessel preparation. Go 27 The other authors used HSV segments oflarger diameter (De of 4.7 mm compared with 3.5 mm in this study) and, because their study focused on the biophysical effects of intraluminal flow, they used 100% oxygen to initially inflate HSV segments to detect vessel leaks. Go 3 However, similar applications of air boluses remove vascular endothelial cells and reduce vascular tone in some cannulated vessel preparations. Go 28 In contrast, because our study focused on evaluating the biologic responses of HSV, we avoided air perfusion and handled vessels cautiously to minimize endothelial or vascular smooth muscle damage. By this method, all HSV in our study constricted to norepinephrine and 5-HT and also showed levels of acetylcholine-induced dilation comparable to those previously measured in HSV mounted for tension-recording studies. Go Go 28,29

It should be noted that the 1 µmol/L concentrations of norepinephrine and 5-HT used in this study represent physiologic levels of these vasoactive agonists, which only submaximally activate HSV segments. Go Go 30,31 For instance, intravascular norepinephrine concentrations as high as 100 µmol/L have been reported in innervated blood vessels, Go 32 whereas 5-HTconcentrations approaching 1 µmol/L have been measured in the effluent from aggregating human platelets. Go 33 Although the same norepinephrine and 5-HT concentrations of 1 µmol/L were used in each experiment, the intensity of vessel responses to vasoactive drugs was variable between veins. This variability in vascular reactivity between vessel segments may be attributed to different ages, genetic profiles, and drug regimens of the patients, as well as to the inherent condition of the vein and the surgical handling of the vessel.

Importantly, our results support the concept that 5-HT is a powerful vasoconstrictor of HSV grafts and a candidate mediator of vasospasm. Go 29 In our studies, 5-HT reduced De and flow of all HSV segments perfused at 90 mm Hg, an effect that was greatly accentuated when pressure was lowered to 70 and 50 mm Hg. The mechanism for this enhanced diameter response to 5-HT at lower pressures was not passive vessel deflation, because vein De was not less at 50 than at 90 mm Hg in agonist-free PSS (Fig. 1, B). Rather, our data suggest that although HSVs are fully distended between 50 and 90 mm Hg, 5-HT is capable of activating venous muscle cells to surmount distending pressures as high as 90 mm Hg, and this activation is more apparent at lower pressures. Norepinephrine also was an effective vasoconstrictor agent, although it only significantly reduced HSV flow at the lower pressures of 70 and 50 mm Hg. This finding is consistent with those of reports from tension-recording studies that norepinephrine is a weaker spasmogen than 5-HT in HSVs. Go 29

Hypotension, graft reactivity, and clinical implications
Isolated HSV segments in this study constricted more strongly to norepinephrine and 5-HT when intraluminal pressures were reduced from 90 mm Hg to levels of 70 or 50 mm Hg. This enhanced vasoconstriction at lower arterial pressures may be interpreted as a mechanism for greater susceptibility to graft vasospasm in patients showing hypotension after aorta-coronary bypass operations. Hypotension is a common complication after aorta-coronary bypass procedures, Go 34 when circulating levels of norepinephrine and 5-HT are increased and platelet aggregation at the graft site may enhance local concentrations of 5-HT. Go Go 6,35 Our study raises the possibility that in the postoperative period the presence of high levels of vasoconstrictor agonists coupled with systemic hypotension may contribute to the induction of graft vasospasm, which can trigger angina and lethal ventricular arrhythmias in some patients. Go Go 4-13 However, in other patients, unless there is spasm of the recipient artery in conjunction with vein spasm, graft vasospasm may go undetected in the postoperative period. Go 6 In these cases, the vascular damage induced by silent episodes of severe vasospasm may present as graft thrombosis at a later date. Go Go Go 5,6,10

Acknowledgments

We thank Ms. Luellen Lougee of LabRat Graphix for the medical illustrations.

Footnotes

From the Human Vascular Biology Laboratory, Department of Physiology, a the Department of Cardiothoracic Surgery, b and the Graduate School Office, c Medical College of Wisconsin, Milwaukee, Wis. Back

References

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T. V. Bilfinger and G. B. Stefano
Human aortocoronary grafts and nitric oxide release: relationship to pulsatile pressure
Ann. Thorac. Surg., February 1, 2000; 69(2): 480 - 485.
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V. Milesi, A. Rebolledo, F. A. Paredes, N. Sanz, J. Tommasi, G. J. Rinaldi, and A. O. Grassi
Mechanical properties of human saphenous veins from normotensive and hypertensive patients
Ann. Thorac. Surg., August 1, 1998; 66(2): 455 - 461.
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T. V. Bilfinger, A. R. Hartman, Y. Liu, H. I. Magazine, and G. B. Stefano
Cryopreserved Veins in Myocardial Revascularization: Possible Mechanism for Their Increased Failure
Ann. Thorac. Surg., April 1, 1997; 63(4): 1063 - 1069.
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