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Ann Thorac Surg 1997;64:1524-1525
© 1997 The Society of Thoracic Surgeons

Correspondence

Nitric Oxide in Homograft Vein Function

Jyotirmay Chanda, MD, Ryosei Kuribayashi, MD, Tadaaki Abe, MD

Department of Cardiovascular Surgery, Akita University School of Medicine, Akita 010, Japan.

To the Editor:

With great interest we read the article by Bilfinger and colleagues published in The Annals [1]. They have concluded that the inability of endothelium to participate in immunovascular process results from failure in modulation of cellular adherence by low nitric oxide (NO) release, which may be one of the possible mechanisms of high early failure rate of cryopreserved vein grafts. In this report no more histologic information is available except partial denudation of endothelium in harvested homograft veins at autopsy.

Nearly two decades have elapsed since Dr Barner [2] "condemned" the use of freeze-preserved saphenous vein allografts for coronary artery bypass because of experimental evidence of "rejection" of such allografts in animals and the unacceptable late mortality rate reported by Tice and associates. In a reply to Barner's "condemnation," Dr Tice [3] claimed that failure occurred in allografts for the same reasons that it occurred in vein autografts, and clinical results of coronary bypass with allografts would appear to be similar to those with vein autografts. Axthelm and colleagues [4] have suggested that both fresh and cryopreserved venous homografts are normally antigenic and a review of available experimental and clinical data suggests that the use of such grafts in patients will be likely to elicit a rejection reaction associated with an unacceptably high graft failure rate. De Caterina and coworkers [5] have already demonstrated that NO reduces the expression of adhesion molecules on the endothelial cells and the recruitment of inflammatory cells, which are a source of growth factors. It is quite understandable that inasmuch as homograft veins are antigenic and endothelium is the primary target of rejection, endothelial NO production would obviously suffer in homograft veins. Autologous saphenous vein grafts are also vulnerable to mechanical denudation of endothelium during handling, resulting in diminished NO production. It is unclear why Bilfinger and colleagues [1] have chosen to perform an experiment on the role of NO in cellular adherence and morphine-stimulated production of NO to define the mechanism of failure of homograft veins, where the immunologic factors predominate. What causes the homograft veins to fail so early after implantation in comparison with autograft veins: nitric oxide? Perhaps not; Bilfinger and associates do not answer this question. Would artificial production of NO prevent occlusion and rejection of homograft veins?

References

  1. Bilfinger TV, Hartman AR, Liu Y, Magazine HI, Stefano GB. Cryopreserved veins in myocardial revascularization: possible mechanism for their increased failure. Ann Thorac Surg 1997;63:1063–9.[Abstract/Free Full Text]
  2. Barner HB. Allogenic saphenous vein for coronary bypass [Letter]. J Thorac Cardiovasc Surg 1978;75:902–3.
  3. Tice DA. Allogenic saphenous vein for coronary bypass. Reply [Letter]. J Thorac Cardiovasc Surg 1978;75:903–4.
  4. Axthelm SC, Porter JM, Strickland S, Baur GM. Antigenicity of venous allografts. Ann Surg 1979;189:290–3.[Medline]
  5. De Caterina R, Libby P, Peng H-B, et al. Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J Clin Invest 1995;76:980–6.
 

Reply

Thomas V. Bilfinger, MD, ScD, Alan R. Hartman, MD, Yu Liu, MD, Harold I. Magazine, PhD, George B. Stefano, PhD

Division of Cardiothoracic Surgery, Cardiac Research Program, State University of New York at Stony Brook, Stony Brook, Ny 11794.

To the Editor:

We appreciate the comments by Chanda and associates. We are well aware of the concerns voiced over time pertaining to cryopreserved veins [1, 2]. We also are well aware of the concept of "slow rejection" that has been forwarded concerning cryopreserved tissues [3]. Yet, there is a considerable difference between the cryopreserved tissue failure rate of valvar conduits versus veins [4]. Because the difference of vein conduits versus internal thoracic artery only appears over years, we looked for a human model with a faster response rate, accepting and agreeing with all the concerns that have been mentioned [5]. Yet, we believe that nitric oxide (NO) has an important role not only in modulation of vascular tone in bypass grafts, as has been shown [6], but also in its ability to decrease the inflammatory response, mainly expressed as cell adherence. What is new in this concept is the fact that endogenous morphine may play an important role in the immunomodulation of NO release [7]. So far the role of endogenous morphine in humans is unknown. This concept fits well with the observation that there is a direct correlation between NO and bypass graft patency [6, 8], and that in native coronary arteries NO donors appear to improve patency and ischemic conditions [9].

References

  1. Iaffaldano RA, Lewis BE, Johnson SA, Piffare R, McKiernan TL. Patency of cryopreserved saphenous vein grafts as conduits for coronary artery bypass surgery. Chest 1995;108:725–9.[Abstract/Free Full Text]
  2. Sellke FW, Stanford W, Rossi NP. Failure of cryopreserved saphenous vein allografts following coronary artery bypass surgery. J Cardiovasc Surg 1991;32:820–3.[Medline]
  3. Bodnar E, Olsen EG, Florio R, Guerreiro D, Ross DN. Heterologous antigenicity induced in human aortic homografts during preservation. Eur J Cardiothorac Surg 1988;2:43–7.[Abstract]
  4. Matsuki O, Robles A, Gibbs S, Bodnar E, Ross DN. Long-term performance of 555 aortic homografts in the aortic position. Ann Thorac Surg 1988;46:187–91.[Abstract]
  5. Goldman S, Zadina K, Krasnicka B, et al. Predictors of graft patency 3 years after coronary bypass graft surgery. J Am Coll Cardiol 1997;19:1563–8.
  6. Luscher TF, Diederich D, Siebenmann R, et al. Difference between endothelium-dependant relaxation in arterial and in venous coronary bypass grafts. N Engl J Med 1988;319:462–7.[Abstract]
  7. Stefano GB, Hartman A, Bilfinger TV, et al. Presence of the µ3 opiate receptor in endothelial cells: coupling to nitric oxide production and vasodilatation. J Biol Chem 1995;270:30290–3.[Abstract/Free Full Text]
  8. Yang Z, Stulz P, von Segesser L, et al. Different interactions of platelets with arterial and venous coronary bypass vessels. Lancet 1991;337:939–43.[Medline]
  9. Sato H, Zhao Z-Q, Jordan JE, et al. Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization. J Thorac Cardiovasc Surg 1997;113:399–409.[Abstract/Free Full Text]



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