title: Effects of elevated perfusion pressure and pulsatile flow on human saphenous veins isolated from diabetic and non-diabetic patients.
abstract: OBJECTIVE
  This study was carried out to determine high pressure and pulsatile flow perfusion effects on human saphenous vein (HSV) segments obtained from diabetic and non-diabetic patients.
  
  
  METHODS
  The veins were perfused with oxygenated Krebs solution for 3 h, with a pulsatile flow rate of 100 mL/min and pressures of 250 × 200 or 300 × 250 mmHg. After perfusion, veins were studied by light microscopy; nitric oxide synthase (NOS) isoforms, CD34 and nitrotyrosine immunohistochemistry and tissue nitrite/nitrate (NO(x)) and malondialdehyde (MDA) quantification.
  
  
  RESULTS
  Light microscopy revealed endothelial denuding areas in all HSV segments subjected to 300 × 250 mmHg perfusion pressure, but the luminal area was similar. The percentage of luminal perimeter covered by endothelium decreased as perfusion pressures increased, and significant differences were observed between groups. The endothelial nitric oxide synthase (eNOS) isoform immunostaining decreased significantly in diabetic patients' veins independent of the perfusion pressure levels. The inducible NOS (iNOS), neuronal NOS (nNOS) and nitrotyrosine immunostaining were similar. Significant CD34 differences were observed between the diabetic 300 × 250 mmHg perfusion pressure group and the non-diabetic control group. Tissue nitrite/nitrate and MDA were not different among groups.
  
  
  CONCLUSIONS
  Pulsatile flow and elevated pressures for 3 h caused morphological changes and decreased the eNOS expression in the diabetic patients' veins.
authors.affiliation: Laboratory of Endothelial Function, Department of Surgery and Anatomy, Ribeirão Preto Faculty of Medicine, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Marina J F
authors.initials: MJ
authors.lastname: Rosique
authors.forename: Rodrigo G
authors.initials: RG
authors.lastname: Rosique
authors.forename: Luis F
authors.initials: LF
authors.lastname: Tirapelli
authors.forename: Edwaldo E
authors.initials: EE
authors.lastname: Joviliano
authors.forename: Marcelo B
authors.initials: MB
authors.lastname: Dalio
authors.forename: Solange
authors.initials: S
authors.lastname: Bassetto
authors.forename: Alfredo J
authors.initials: AJ
authors.lastname: Rodrigues
authors.forename: Paulo R B
authors.initials: PR
authors.lastname: Evora
mesh_terms: D000368:Aged; D018952:Antigens, CD34 / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D015536:Down-Regulation; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications*; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010477:Perfusion; D011312:Pressure / Q000009:adverse effects; D011673:Pulsatile Flow; D012501:Saphenous Vein / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects; D014680:Veins / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018952:Antigens, CD34; C496320:NOS1 protein, human; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III