title: Enhancement of endothelial function by pregnancy: inadequate response in women with type 1 diabetes.
abstract: OBJECTIVE
  Pregnant women with type 1 diabetes have a substantially increased risk of vascular complications. Our aim was to study vascular function and metabolic and inflammatory risk factors during the antenatal and postpartum periods in women with type 1 diabetes compared with healthy control subjects.
  
  
  METHODS
  A total of 15 women with diabetes and 30 control subjects were recruited in the third trimester of pregnancy. Of these women, 9 case subjects and 16 control subjects were reinvestigated in the postnatal period. Blood samples were collected and microvascular skin perfusion was assessed in vivo using laser Doppler imaging and iontophoretic administration of endothelial-dependent (acetylcholine [ACH]) and endothelial-independent (sodium nitroprusside [SNP]) vasodilators.
  
  
  RESULTS
  Microvascular responses in both control subjects (ACH, P = 0.018; SNP, P = 0.01) and diabetic women (ACH, P = 0.029; SNP, P = 0.105) were better during pregnancy than in the postnatal period, although responses in women with diabetes were significantly inferior to those in control subjects during both periods (all P < 0.001, two-way ANOVA). This dysfunction existed despite similar lipoprotein profiles. The difference in vascular responsivity between case and control subjects was significantly attenuated by adjustment for differences in HbA(1c) but not C-reactive protein concentrations in the two groups.
  
  
  CONCLUSIONS
  Pregnancy enhances microvascular function, but in women with diabetes, such improvements are insufficient to attain responses seen in healthy nonpregnant women. This suggests a persistent vascular defect in young women with type 1 diabetes that may contribute to adverse pregnancy outcome. Our data suggest a role for the chronic effects of hyperglycemia in the impaired vascular responsiveness in such women.
authors.affiliation: University Department of Obstetrics and Gynaecology, Glasgow Royal Infirmary, Scotland, UK. jer6q@clinmed.gla.ac.uk
authors.forename: Jane E
authors.initials: JE
authors.lastname: Ramsay
authors.forename: Roslyn J
authors.initials: RJ
authors.lastname: Simms
authors.forename: William R
authors.initials: WR
authors.lastname: Ferrell
authors.forename: Lynn
authors.initials: L
authors.lastname: Crawford
authors.forename: Ian A
authors.initials: IA
authors.lastname: Greer
authors.forename: Mary-Anne
authors.initials: MA
authors.lastname: Lumsden
authors.forename: Naveed
authors.initials: N
authors.lastname: Sattar
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D019540:Area Under Curve; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D008833:Microcirculation / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D049590:Postpartum Period; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D011254:Pregnancy in Diabetics / Q000503:physiopathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000109:Acetylcholine; D001786:Blood Glucose; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D009599:Nitroprusside; D019010:Vascular Cell Adhesion Molecule-1; D014665:Vasodilator Agents