open access

Vol 81, No 3 (2022)
Original article
Submitted: 2021-05-06
Accepted: 2021-07-26
Published online: 2021-08-24
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Morphologic comparison of blood vessels used for coronary artery bypass graft surgery

M. Garnizone1, E. Vartina1, M. Pilmane1
·
Pubmed: 34608982
·
Folia Morphol 2022;81(3):584-593.
Affiliations
  1. Department of Morphology, Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia

open access

Vol 81, No 3 (2022)
ORIGINAL ARTICLES
Submitted: 2021-05-06
Accepted: 2021-07-26
Published online: 2021-08-24

Abstract

Background: The aim of this study was to evaluate morphologic features of healthy saphenous vein and internal thoracic artery, blood vessels used in coronary artery bypass graft (CABG) surgery, and compare results.
Materials and methods: Ten specimens of saphenous veins and ten of internal thoracic arteries used for CABG were obtained from 20 patients. Histological routine and immunohistochemical staining was performed with: endothelin (ET), tissue inhibitor of metalloproteinase 2 (TIMP2), metallomembranoproteinase 2 (MMP2), transforming growth factor beta (TGFβ), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP9.5), vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM). A semiquantitative evaluation method was used.
Results: There was found: a moderate number of endothelin-positive cells in both blood vessel types; a moderate number of MMP2-positive cells and moderate in number to numerous TIMP2-positive cells in veins. In arteries — occasionally marked positive MMP2 cells and negative TIMP2; moderate in number to numerous VEGF-positive endothelial cells on small blood vessels in vein wall and occasionally in artery wall; numerous TGFβ-positive structures in veins and abundance of VCAM- and ICAM-positive cells, few in arteries; few HGF-positive structures in veins, negative in arteries; In veins, few PGP9.5-positive nerve fibres, in arteries — moderate. Moderate TUNEL reaction-positive apoptotic cells in veins and few to moderate in arteries.
Conclusions: Vena saphena magna grafts are characterised by increased plasticity when it comes to modelling. Number of VEGF, VCAM and ICAM found in vena saphena magna proves the possible tendency of graft failure on basis of local blood supply intensification. Appearance of endothelin positive cells indicate the similar homeostasis condition in endotheliocytes in both — vein and artery grafts.

Abstract

Background: The aim of this study was to evaluate morphologic features of healthy saphenous vein and internal thoracic artery, blood vessels used in coronary artery bypass graft (CABG) surgery, and compare results.
Materials and methods: Ten specimens of saphenous veins and ten of internal thoracic arteries used for CABG were obtained from 20 patients. Histological routine and immunohistochemical staining was performed with: endothelin (ET), tissue inhibitor of metalloproteinase 2 (TIMP2), metallomembranoproteinase 2 (MMP2), transforming growth factor beta (TGFβ), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP9.5), vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM). A semiquantitative evaluation method was used.
Results: There was found: a moderate number of endothelin-positive cells in both blood vessel types; a moderate number of MMP2-positive cells and moderate in number to numerous TIMP2-positive cells in veins. In arteries — occasionally marked positive MMP2 cells and negative TIMP2; moderate in number to numerous VEGF-positive endothelial cells on small blood vessels in vein wall and occasionally in artery wall; numerous TGFβ-positive structures in veins and abundance of VCAM- and ICAM-positive cells, few in arteries; few HGF-positive structures in veins, negative in arteries; In veins, few PGP9.5-positive nerve fibres, in arteries — moderate. Moderate TUNEL reaction-positive apoptotic cells in veins and few to moderate in arteries.
Conclusions: Vena saphena magna grafts are characterised by increased plasticity when it comes to modelling. Number of VEGF, VCAM and ICAM found in vena saphena magna proves the possible tendency of graft failure on basis of local blood supply intensification. Appearance of endothelin positive cells indicate the similar homeostasis condition in endotheliocytes in both — vein and artery grafts.

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Keywords

immunohistochemistry, saphenous vein, internal thoracic artery

About this article
Title

Morphologic comparison of blood vessels used for coronary artery bypass graft surgery

Journal

Folia Morphologica

Issue

Vol 81, No 3 (2022)

Article type

Original article

Pages

584-593

Published online

2021-08-24

Page views

4684

Article views/downloads

901

DOI

10.5603/FM.a2021.0084

Pubmed

34608982

Bibliographic record

Folia Morphol 2022;81(3):584-593.

Keywords

immunohistochemistry
saphenous vein
internal thoracic artery

Authors

M. Garnizone
E. Vartina
M. Pilmane

References (53)
  1. Abraham D, Dashwood M. Endothelin: role in vascular disease. Rheumatology (Oxford). 2008; 47 Suppl 5: v23–v24.
  2. Airhart N, Curci JA. Arterial Aneurysms. In: Cronenwett JL, Johnston KW (ed). Rutherford's Vascular Surgery 8th ed. Elsevier, London, UK 2014: 113–131.
  3. Allen S, Khan S, Tam Sp, et al. Expression of adhesion molecules by lp(a): a potential novel mechanism for its atherogenicity. FASEB J. 1998; 12(15): 1765–1776.
  4. Anstadt MP, Franga DL, Portik-Dobos V, et al. Native matrix metalloproteinase characteristics may influence early stenosis of venous versus arterial coronary artery bypass grafting conduits. Chest. 2004; 125(5): 1853–1858.
  5. Baron SJ, Mick S, Shekar PS, Mauri I. Cardiovascular Therapeutics: A Companion to Braunwald's Heart Disease. In: Antman EM, Sabatine MS (ed). 4th Ed. W.B. Saunders 2013: 214–239.
  6. Berceli SA. Autogenous Grafts. In: Cronenwett JL, Johnston KW (ed). Rutherford's Vascular Surgery. 8th ed. Elsevier, London, UK 2014: 1382–1401.
  7. Breier G, Albrecht U, Sterrer S, et al. Expression of vascular endothelial growth factor during embryonic angiogenesis and endothelial cell differentiation. Development. 1992; 114(2): 521–532.
  8. Broide DH, Sriramarao P. Cellular Adhesion in Inflammation. In: Franklin Adkinson JrN (ed). Middleton's Allergy: Principles and Practice 8th ed. Elsevier, Philadelphia, USA 2013: 81–94.
  9. Buratto E, Shi WY, Konstantinov IE. An intima affair adds to the dominion of the internal thoracic artery in coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2016; 151(6): 1709–1710.
  10. Cho A, Courtman DW, Langille BL. Apoptosis (programmed cell death) in arteries of the neonatal lamb. Circ Res. 1995; 76(2): 168–175.
  11. Cox J, Chiasson D, Gotlieb A. Stranger in a strange land: The pathogenesis of saphenous vein graft stenosis with emphasis on structural and functional differences between veins and arteries. Prog Cardiovasc Dis. 1991; 34(1): 45–68.
  12. Danik JS, Paynter NP, Ridker PM. Genomic Biomarkers in Human Population Studies. In: Ginsburg GS, Huntington WF (ed). Genomic and Personalized Medicine 2nd ed. Academic Press, UK, London 2012: 247–262.
  13. Dvorak HF, Brown LF, Detmar M, et al. Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis. Am J Pathol. 1995; 146(5): 1029–1039.
  14. Freischlag JA, Heller JA. Venous disease. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL (ed). Sabiston Textbook of Surgery. 20th ed., Elsevier, Philadelphia, USA 2016: 1827–1847.
  15. Galis ZS, Johnson C, Godin D, et al. Targeted disruption of the matrix metalloproteinase-9 gene impairs smooth muscle cell migration and geometrical arterial remodeling. Circ Res. 2002; 91(9): 852–859.
  16. Galis Z, Khatri J. Matrix metalloproteinases in vascular remodeling and atherogenesis. Circulation Res. 2002; 90(3): 251–262.
  17. Gallagher PJ, van der Wal AC. Cardiovascular system. In: Cross S (ed). Underwood's Pathology: A Clinical Approach. 6th ed. Elsevier, London, UK 2013: 242–283.
  18. Gulbenkian S, Wharton J, Polak JM. The visualisation of cardiovascular innervation in the guinea pig using antiserum to protein gene product 9.5 (pgp 9.5). J Autonomic Nervous System. 1987; 18(3): 235–247.
  19. Halabi AR, Alexander JH, Shaw LK, et al. Relation of early saphenous vein graft failure to outcomes following coronary artery bypass surgery. Am J Cardiol. 2005; 96(9): 1254–1259.
  20. Havelka GE, Kibbe MR. The vascular adventitia: its role in the arterial injury response. Vasc Endovascular Surg. 2011; 45(5): 381–390.
  21. Hinokiyama K, Valen G, Tokuno S, et al. Vein graft harvesting induces inflammation and impairs vessel reactivity. Ann Thorac Surg. 2006; 82(4): 1458–1464.
  22. Hocking KM, Brophy C, Rizvi SZ, et al. Detrimental effects of mechanical stretch on smooth muscle function in saphenous veins. J Vasc Surg. 2011; 53(2): 454–460.
  23. Kanzaki T, Tamura K, Takahashi K, et al. In vivo effect of TGF- beta 1. Enhanced intimal thickening by administration of TGF- beta 1 in rabbit arteries injured with a balloon catheter. Arterioscler Thromb Vasc Biol. 1995; 15(11): 1951–1957.
  24. Kon Y, Endoh D, Iwanaga T. Expression of protein gene product 9.5, a neuronal ubiquitin C-terminal hydrolase, and its developing change in Sertoli cells of mouse testis. Mol Reprod Develop. 1999; 54(4): 333–341, doi: 10.1002/(sici)1098-2795(199912)54:4<333::aid-mrd3>3.0.co;2-8.
  25. Kovacević M, Simić O, Jonjić N, et al. Apoptosis and cardiopulmonary bypass. J Card Surg. 2007; 22(2): 129–134.
  26. Kyrylkova K, Kyryachenko S, Leid M, et al. Detection of apoptosis by TUNEL assay. Methods Mol Biol. 2012; 887: 41–47.
  27. Ley K, Huo Y. VCAM-1 is critical in atherosclerosis. J Clin Invest. 2001; 107(10): 1209–1210.
  28. Lönn J, Starkhammar Johansson C, Kälvegren H, et al. Hepatocyte growth factor in patients with coronary artery disease and its relation to periodontal condition. Results Immunol. 2011; 2: 7–12.
  29. Low EL, Baker AH, Bradshaw AC. Dissecting transforming growth factor-beta signalling pathways in primary human vascular smooth muscle cells. Atherosclerosis. 2015; 241(1): e77.
  30. Lu F, Zhao X, Wu J, et al. MSCs transfected with hepatocyte growth factor or vascular endothelial growth factor improve cardiac function in the infarcted porcine heart by increasing angiogenesis and reducing fibrosis. Int J Cardiol. 2013; 167(6): 2524–2532.
  31. Maiellaro K, Taylor WR. The role of the adventitia in vascular inflammation. Cardiovasc Res. 2007; 75(4): 640–648.
  32. Mallat Z, Tedgui A. Apoptosis in the vasculature: mechanisms and functional importance. Br J Pharmacol. 2000; 130(5): 947–962.
  33. Martinez-Lemus L, Galiñanes E. Matrix metalloproteinases and small artery remodeling. Drug Discovery Today: Disease Models. 2011; 8(1): 21–28.
  34. Meng X, Fu Q, Sun W, et al. Competitive flow arising from varying degrees of coronary artery stenosis affects the blood flow and the production of nitric oxide and endothelin in the internal mammary artery graft. Eur J Cardiothorac Surg. 2013; 43(5): 1022–1027.
  35. Nagase H, Visse R, Murphy G. Structure and function of matrix metalloproteinases and TIMPs. Cardiovasc Res. 2006; 69(3): 562–573.
  36. Nordgaard H, Nordhaug D, Kirkeby-Garstad I, et al. Different graft flow patterns due to competitive flow or stenosis in the coronary anastomosis assessed by transit-time flowmetry in a porcine model. Eur J Cardiothorac Surg. 2009; 36(1): 137–142.
  37. Ovalle WK, Nahirney PC. Cardiovascular system. In:, Nahirney PC (ed). Netter's Essential Histology. 2nd ed. . Elsevier, London, UK 2013: 187–209.
  38. Pilmane M, Luts A, Sundler F. Changes in neuroendocrine elements in bronchial mucosa in chronic lung disease in adults. Thorax. 1995; 50(5): 551–554.
  39. Schiffrin EL. Role of endothelin-1 in hypertension. Hypertension. 1999; 34: 876–881.
  40. Schwartz SM, deBlois D, O'Brien ER. The intima. Soil for atherosclerosis and restenosis. Circ Res. 1995; 77(3): 445–465.
  41. Shyu KG, Chang ML, Wang BW, et al. Cyclical mechanical stretching increases the expression of vascular endothelial growth factor in rat vascular smooth muscle cells. J Formos Med Assoc. 2001; 100(11): 741–747.
  42. Sims F. The initiation of intimal thickening in human arteries. Pathology. 2000; 32(3): 171–175.
  43. Smith M, Long D, Damiano E, et al. Near-Wall μ-PIV reveals a hydrodynamically relevant endothelial surface layer in venules in vivo. Biophysical J. 2003; 85(1): 637–645.
  44. Stefanini M, De Martino C, Zamboni L. Fixation of ejaculated spermatozoa for electron microscopy. Nature. 1967; 216(5111): 173–174.
  45. Sumpio B, Chin J. Vessel Wall Biology. In: Sidawy AN, Perler BA (ed). Rutherford's Vascular Surgery and Endovascular Therapy. 9th ed. Elsevier, Philadelphia, USA 2018: 30–43.
  46. Trindade M, Oigman W, Fritsch Neves M. Potential role of endothelin in early vascular aging. Curr Hypertens Rev. 2017; 13(1): 33–40.
  47. Tykocki NR, Gariepy CE, Watts SW. Endothelin ET(B) receptors in arteries and veins: multiple actions in the vein. J Pharmacol Exp Ther. 2009; 329(3): 875–881.
  48. Velazquez O, Wang B. Cells of the Vascular System. In: Cronenwett JL, Johnston KW (ed). Rutherford's Vascular Surgery 8th ed. Elsevier, London, UK 2014: 49–65.
  49. Wei W, Chen ZW, Yang Q, et al. Vasorelaxation induced by vascular endothelial growth factor in the human internal mammary artery and radial artery. Vascul Pharmacol. 2007; 46(4): 253–259.
  50. Wolinsky H, Glagov S. A lamellar unit of aortic medial structure and function in mammals. Circ Res. 1967; 20(1): 99–111.
  51. Yu P, Nguyen BT, Tao M, et al. Lack of interleukin-1 signaling results in perturbed early vein graft wall adaptations. Surgery. 2013; 153(1): 63–69.
  52. Yuan SM, Wang YQ, Shen Yi, et al. Transforming growth factor-beta in graft vessels: histology and immunohistochemistry. Clinics (Sao Paulo). 2011; 66(5): 895–901.
  53. Yung LM, Nikolic I, Paskin-Flerlage SD, et al. A selective transforming growth factor-β ligand trap attenuates pulmonary hypertension. Am J Respir Crit Care Med. 2016; 194(9): 1140–1151.

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