title: Structural, biochemical and functional effects of distending pressure in the human saphenous vein: implications for bypass grafting.
abstract: BACKGROUND
  Distension of the saphenous vein before and after coronary artery bypass grafting results in damage to mechanisms that regulate vascular tone. We have investigated the relationship between the magnitude of distending pressure and the degree of structural, biochemical and functional damage to the vessel wall.
  
  
  METHODS
  Vessel segments that had been distended to either 100 or 300 mmHg were set up in isolated organ baths and the function of the smooth muscle and endothelial cells examined. All segments examined were then fixed for assessment of structural damage by scanning electron microscopy and for immunocytochemical localisation of endothelial nitric oxide synthase.
  
  
  RESULTS
  Segments of saphenous vein distended to 100 mmHg retained their responsiveness to KCl (90 mmol/l) and phenylephrine (10(-6) mol/l), but those pressurised to 300 mmHg had significantly reduced responses to both agents. There was also a significant reduction in response to the endothelium-dependent dilators, acetylcholine (10(-10)-10(-6) mol/l) and bradykinin (10(-10)-10(-6) mol/l) in those segments distended to 300 mmHg. Quantitative studies of structural endothelial damage showed a significant loss of endothelium at 300 mmHg distension pressure. Remaining endothelial cells retained strong positive staining for endothelial nitric oxide synthase. By electron microscopic examination, those vessels distended to 100 mmHg showed lifting and rounding of individual cells, whereas segments distended to 300 mmHg revealed major areas of denuded endothelium.
  
  
  CONCLUSIONS
  Distension of saphenous veins to pressures equivalent to those in the systemic circulation result in structural and biochemical changes in the endothelium that are not paralleled by immediate functional vasomotor changes.
authors.affiliation: Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, Harefield Hospital, UK.
authors.forename: A H
authors.initials: AH
authors.lastname: Chester
authors.forename: L D
authors.initials: LD
authors.lastname: Buttery
authors.forename: J A
authors.initials: JA
authors.lastname: Borland
authors.forename: D R
authors.initials: DR
authors.lastname: Springall
authors.forename: S
authors.initials: S
authors.lastname: Rothery
authors.forename: N J
authors.initials: NJ
authors.lastname: Severs
authors.forename: J M
authors.initials: JM
authors.lastname: Polak
authors.forename: M H
authors.initials: MH
authors.lastname: Yacoub
mesh_terms: D000368:Aged; D001026:Coronary Artery Bypass / Q000009:adverse effects*; D003327:Coronary Disease / Q000601:surgery; D046508:Culture Techniques; D004106:Dilatation / Q000009:adverse effects; D004730:Endothelium, Vascular / Q000378:metabolism / Q000648:ultrastructure*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008855:Microscopy, Electron, Scanning; D008875:Middle Aged; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D011312:Pressure; D012016:Reference Values; D012501:Saphenous Vein / Q000201:enzymology* / Q000473:pathology* / Q000637:transplantation; D014654:Vascular Patency / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D019001:Nitric Oxide Synthase