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Ann Thorac Surg 2001;71:133-137
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Direct measurement of nitric oxide release from saphenous vein: abolishment by surgical preparation

^a Cardiovascular Research Laboratory, Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China
^b Starr Academic Center, Providence Heart Institute, Portland, Oregon, USA

Accepted for publication July 18, 2000.

Address reprint requests to Dr He, Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Block B, 5A, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China
e-mail: gwhe{at}cuhk.edu.hk

	Abstract

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Background. Surgical preparation (distension) of the saphenous vein (SV) is applied routinely during harvesting in coronary artery bypass grafting (CABG). However, mechanical distension may impair the endothelium, which plays an important role in long-term patency. The present study investigated the effect of surgical preparation of the SV on nitric oxide (NO) release from the endothelium by direct measurement of NO.

Methods. Saphenous vein segments taken from CABG patients were cut open longitudinally and placed in an organ chamber. An NO-sensitive electrode and NO meter were used to directly measure NO release induced by acetylcholine (ACh) and bradykinin (BK) from the surgically prepared veins (PV) compared with the control (nondistended) veins.

Results. The basal release of NO in the PV group was significantly lower than that in the control group (3.4 ± 1.4 nM, n = 9 versus 9.9 ± 2.8 nM, n = 13, p = 0.002). The maximum concentrations of NO release induced by ACh and BK in the PV group were also significantly lower than those in the control veins (for ACh 10^-6 mol/L: 9.6 ± 3.1 nM, n = 8 versus 41.9 ± 11.2 nM, n = 12, p = 0.005; for BK 10^-8 mol/L: 8.3 ± 3.7 nM, n = 7 versus 37.9 ± 6.1 nM, n = 9, p = 0.003). Further, the duration of NO release in the PV group was significantly shorter than that in control veins (1.5 ± 1.3 minutes, n = 8 versus 8.1 ± 1.9 minutes, n = 8, p < 0.001).

Conclusions. Surgical preparation almost abolishes NO release by the SV and this may significantly contribute to the low long-term patency rate of the vein graft.

	Introduction

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Graft failure is one of the major causes of recurrent angina after coronary artery bypass grafting (CABG). It has been demonstrated that the long-term patency rate of vein grafts is poor compared with the internal mammary artery (IMA) graft [1]. The occlusion rate of saphenous vein (SV) grafts in the first year is 10% to 26% [2, 3]. By 10 years, 50% of the grafts are occluded [4, 5] and, of the grafts still patent, 50% showed marked atherosclerotic change [4]. There is evidence showing that the damages resulting from some deleterious interventions to overcome spasm of SV during harvesting and the exposure of vein grafts to a high arterial pressure account for, at least in part, the consequences [6, 7]. These interventions include surgical preparation (high-pressure distension and handling) [6, 7], the detrimental effects of some antispastic agents [8], and inappropriate solution for flushing and storing the vein graft.

Surgical preparation is still a routine method used in SV harvesting. It is apparent that overdistension of SV will cause damage to both the endothelium and the media of the vascular wall [9]. Because of the critical role the vascular endothelium plays [10], the endothelial function of the coronary bypass grafts is crucial to the long-term graft patency.

Nitric oxide (NO) is the major autacoid generated by the endothelial cells and plays a central role in the regulation of vascular tone and homeostasis [11]. Previous studies have shown that surgical preparation of SV impairs the endothelium-dependent relaxation [12, 13]. In addition, in our laboratory we have demonstrated that surgical preparation abolishes the endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization of the smooth muscle cells of SV [14]. However, the influence of surgical preparation on NO release by means of direct measurement of NO has never been reported. The present study was therefore designed to evaluate the effects of surgical preparation of SV on NO release by directly measuring the NO released from the endothelium of SV.

	Material and methods

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Vessel preparation
Human SV segments were harvested from patients undergoing CABG. Approval to use discarded SV tissue was given by the Ethics Committee of Grantham Hospital. Segments of veins before surgical preparation were taken as a control. The surgical procedure of the vein harvesting followed the traditional method and was randomly carried out by assistant surgeons. Leg incisions were made along the length of the SV and the SV was fully exposed. The SV was dissected carefully and the branches were ligated by silk ties. The veins were than distended by injecting heparinized lactate Ringer’s solution to check diameter and leakage and to overcome spasm that is frequently encountered. The pressure used for distension was not particularly measured during operation. However, in the laboratory setting, it was determined that the pressure required to distend the vein varied from 100 to 600 mm Hg. The required length was measured. The required vein was taken out from the leg and stored in the lactate Ringer’s solution at room temperature for grafting. The redundant vein segments were resected, immediately placed in 4°C Krebs’ solution (see below), and transferred to the laboratory. The vessels were placed in a glass dish filled with Krebs’ solution and dissected free from surrounding fat and connective tissue. All vessels were cut into 5 mm long rings and opened longitudinally and then fixed on the bottom of an organ chamber (volume = 3 mL) with the endothelium side upward. The organ chamber was continuously superfused with Krebs’ solution bubbled with 95% O₂ and 5% CO₂ at a constant rate of 3 mL/min and the temperature was maintained at 37°C. The compositions of Krebs’ solution are as follows (in mM): Na⁺ 144; K⁺ 5.9; Ca²⁺ 2.5; Mg²⁺ 1.2; Cl^- 128.7; HCO₃^- 25; SO₄^2- 1.2; H₂PO₄^- 1.2; glucose 11. After 60 minutes of incubation the following procedures were performed.

Direct measurement of NO
The membrane-type, NO-sensitive electrode (ISO-NOP, World Precision Instrument [WPI], Inc, Sarasota, FL) and isolated NO meter (ISO-NO Mark II, WPI, Inc) were used to measure the isolated NO generated by the vascular endothelium. The detection of NO is an electrochemical method in which a potential is applied to the measuring electrode relative to the reference electrode and the resulting current due to the electrochemical oxidation of NO is monitored. The membrane-type, NO-sensitive electrode consists of a working electrode covered by a gas-permeable membrane. Nitric oxide diffuses through the selective membrane or coatings and is oxidized on the surface of the prepolarized electrode, resulting in an electrical current. The magnitude of the redox current is in direct proportion to the concentration of NO in the sample and is amplified by the NO meter and registered by a computer (Duo•18 data recording system, WPI, Inc).

Selectivity of NO-sensitive electrodes
The selectivity of the ISO-NOP electrode was tested in connection with calibration, where a lack of response to strong saline solution (3M) or sodium nitrate (NaNO₂) up to 100 µM was taken as evidence for an intact coating of the electrode. The electrodes did not respond to acetylcholine (ACh; 10 µM), bradykinin (BK; 1 µM), indomethacin (7 µM), N^G-nitro-L-arginine (L-NNA; 300 µM), and oxyhemoglobin (20 µM), which were added into the calibration glass vial. The calibration of the instrument followed the standardized procedure [15]. The calibration was performed daily before the experiment.

There are two environmental variables that the instrument is inherently sensitive to due to its electrochemical nature and they are critical to the successful measurement of NO. These are temperature and electrical interference. Therefore, the environmental temperature was kept strictly constant and the instrument was properly grounded and shielded by a Faraday cage.

Measurement of NO
After calibration, the NO-sensitive electrode was inserted into the organ chamber vertically and placed as close to the endothelial surface as possible by means of a micromanipulator (WR-6, Narishige International, Tokyo, Japan). The NO electrode was connected to the amplifier (NO meter, ISO-NO Mark II, WPI, Inc) and the NO signals were recorded. After 60 to 120 minutes of equilibration of each vein segment in the organ chamber, the electrode was stabilized and the baseline of the current became stable. The measurement of NO was carried out.

The NO concentration measured with the NO-sensitive electrode reflects the NO released from the endothelium minus NO that has been clearanced by degradation and diffusion.

Experimental protocol
To investigate the different capacity of NO generation and release of the surgically prepared (dilated) SV (PV) and normal (not dilated) SV, ACh-induced NO release and BK-induced NO release in the PV segments (n = 16) and normal SV segments (control, n = 16) were examined. After 60 minutes of incubation and equilibration of each vein segment in the organ chamber, cumulative doses of ACh (-8 to -5 log mol/L) or BK (-10 to -7 log mol/L) were added to the organ chamber and the NO signals were recorded. The interval between each addition of the different concentration of ACh or BK was 15 minutes. The organ chamber was then washed with Krebs’ solution. N^G-nitro-L-arginine (300 µM), an NO biosynthesis inhibitor, indomethacin (7 µM), a cyclooxygenase inhibitor, and oxyhemoglobin (20 µM), the NO scavenger, were added into the organ chamber. After incubation and equilibration for another 60 minutes, the steps mentioned above were repeated.

Data analysis
All results are expressed as means ± standard error of the mean. When the comparison was made between intact veins and surgically prepared ones, the unpaired Student’s t test was used. A value of p less than 0.05 was considered significant.

Drugs
Acetylcholine HCl, BK, potassium nitrite (KNO₂), potassium iodide (KI), L-NNA, indomethacin, and oxyhemoglobin were purchased from Sigma (St. Louis, MO). The drugs were prepared in distilled water except for indomethacin, which was dissolved in ethanol.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Calibrations
The ISO-NOP electrodes responded with increases in current to nanomolar concentrations of NO. The electrode was calibrated by the chemical generation of NO as described above. The magnitude of the output current of the electrode correlates linearly with the concentration of NO (r = 0.997 ± 0.002, n = 36, p < 0.001).

Direct measurement of NO release
Basal release of NO
The basal level of NO release in the organ chamber measured in the PV group was significantly less than that in control veins (3.4 ± 1.4 nM, n = 9 versus 9.9 ± 2.8 nM, n = 13, p = 0.0018; Fig 1).

View larger version (12K): [in this window] [in a new window]   Fig 1. The basal release of nitric oxide (NO) in the surgically prepared veins (PV; n = 9) and normal saphenous veins (SV; n = 13). Values are means ± standard error of the mean. *p < 0.005, PV versus SV.

View larger version (17K): [in this window] [in a new window]   Fig 2. Representative recordings (right to left) of nitric oxide release from the normal saphenous veins (SV) and surgically prepared veins (PV) when bradykinin (BK; in log mol/L) was applied (indicated by arrows). In the endothelium-denuded segments (E-) of both normal saphenous veins and surgically prepared veins, nitric oxide could not be detected.

View larger version (16K): [in this window] [in a new window]   Fig 3. The stimulated release of nitric oxide in the surgically prepared veins (PV) and normal saphenous veins (SV). The maximal release of nitric oxide induced by acetylcholine (ACh; A) and bradykinin (BK; B) in the PV group (n = 8) was significantly lower than that in the SV group (A: n = 12; B: n = 9). Values are presented as means ± standard error of the mean. *p < 0.05, **p < 0.01, PV versus SV.

View larger version (16K): [in this window] [in a new window]   Fig 4. The concentration-time curves of nitric oxide (NO) release elicited by bradykinin of -7 log mol/L in the surgically prepared veins (PV) and normal saphenous veins (SV). The duration of NO release in the PV was significantly shorter than that in SV (p < 0.001). The results are the means of eight experiments and the horizontal bars represent standard error of the mean. *p < 0.05, **p < 0.01, PV versus SV.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The present study demonstrated that both basal and stimulated release of NO in surgically prepared veins are almost abolished compared with normal SV. This may significantly contribute to the poor long-term patency rate of the vein graft.

Since the initial discovery of the endothelium-derived relaxing factor [10], which was identified later as NO, it has become more and more clear that NO is the most important endothelium-derived autacoid. In addition to the modulation of vascular tone, NO has many vasoprotective properties such as inhibition of platelet and neutrophil aggregation and adhesion and arrest of smooth muscle cell proliferation [15, 16]. These effects of NO are the essential mechanisms against vessel occlusion. Moreover, NO may exert an influence on the production of other endothelium-derived autacoids such as prostacyclin and EDHF in vitro and in vivo [17, 18]. Therefore, loss of the ability to produce and release NO means loss of the vascular protective mechanism.

SV is still used extensively as a bypass graft in CABG, even though the long-term patency rate of the vein graft is inferior to that of IMA grafts. The poor long-term patency of SV grafts has been attributed to the structural and functional characteristics of the vascular wall and endothelium of SV [19]. However, studies have shown that SV grafts remain reactive to vessel dilator stimuli for up to 10 to 20 years [20, 21]. This may suggest that proper protection of SV grafts during harvesting may improve the long-term results.

Much evidence has been acquired concerning the adverse effects of distending SV grafts at a high pressure during preparation for grafting. The method we use to distend the vein graft during operation is commonly used in most cardiac surgical units. Studies showed that the early effects of excessive distension are degenerative changes in the vascular wall [6], damage of both smooth muscle and media [6, 22], loss of endothelium, reduced fibrinolytic activity [23], and exposure of subintimal tissue to the blood, which in turn causes deposition of platelets and fibrin. Platelets release growth factor that stimulate proliferation of smooth muscle cells in the subintimal tissue. Even though the endothelial cover is reestablished, there are still permanent structural changes in the vein wall visible as an area of neointimal thickening and reduction in lumen diameter [6]. The long-term effect of these events is increased local uptake of plasma lipids [24], which most likely predisposes the vein graft in the atherosclerosis and occlusion finally.

In the present study, we directly measured NO release in the SV. We found that after surgical preparation of SV, both basal and stimulated NO release, especially the capacity of continuous release of NO, were significantly attenuated compared with the normal veins. Our study together with the previous ones [9, 12–14] suggest that the surgical preparation may contribute significantly to the poor long-term patency of the vein graft.

It has been reported that constitutive NO synthase is expressed and NO-mediated relaxation is preserved in retrieved human aortocoronary vein grafts [12]. This indicates that the endothelial function could be restored and preserved for a longer period in the grafts in which endothelium damage is less severe. In other words, the different degree of endothelial damage due to different extent of vein distension may result in a different long-term outcome of the vein grafts. Indeed, the pressure applied to dilate the spastic vein is usually much higher than the arterial pressure [9]. This implies that the high-pressure dilatation may cause more serious damage to the endothelium and vascular wall than the damage caused by exposure of vein graft to arterial pressure, particularly when saline is used [25]. Our previous study has shown that pharmacologic dilatation of the SV could result in a satisfactory relaxation and avoid the necessity for high-pressure distension [26] and therefore will not cause endothelial injury. Although we did not directly study the effect of low-pressure distension on NO release, we previously demonstrated that low-pressure distension under pharmacologic methods preserves the endothelium-dependent relaxation, which is indirect evidence of the preservation of NO production [26]. In the sense of endothelial preservation and better long-term graft patency, pharmacologic preparation of SV should be used during harvesting of the SV.

In conclusion, our study by direct measurement of NO release from the endothelium demonstrates that surgical preparation reduces or abolishes the ability of the endothelium to release NO. This may significantly contribute to the poor long-term patency of the SV graft. Appropriate preparation of SV grafts during harvesting may significantly improve the long-term results of CABG using SV grafts.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was supported by grants from the Hong Kong Research Grants Council (CUHK7280/97M and 7246/99M). Doctor Z.-G. Liu is a Visiting Fellow and Dr X.-C. Liu is from the Department of Cardiac Surgery, Peking Union Medical College. The experimental work was performed at the Cardiovascular Research Laboratory, Grantham Hospital, headed by Professor G.-W. He.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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