title: Better preservation of endothelial function and decreased activation of the fetal renin-angiotensin pathway with the use of pulsatile flow during experimental fetal bypass.
abstract: OBJECTIVE
  Pulsatile flow was shown to overcome the progressive rise in peripheral and placental vascular resistances observed during steady-flow bypass, this rise being counteracted by inhibition of nitric oxide synthase. This study quantifies the release of endothelial vasoactive substances during a 60-minute in utero model of fetal bypass.
  
  
  METHODS
  Fetuses were randomly allocated into 1 of 2 groups (steady flow, n = 8, or pulsatile flow, n = 13) and subjected to bypass through central cannulation and perfusion with either a centrifugal or pulsatile (125 beats x min(-1)) blood pump.
  
  
  RESULTS
  Lactate concentration was high, starting at fetal exteriorization and increasing during fetal preparation in the 2 groups. Once bypass was established, the rise was significant only in the steady-flow group. Plasma nitric oxide metabolites, similar before bypass, reached higher levels during pulsatile flow at the end of bypass (99+/-9 vs. 82+/-23 micromol x L(-1); P =.037). Levels of urinary nitric oxide metabolites were significantly higher in the pulsatile-flow than in the steady-flow group (764+/-143 vs. 508+/-240 micromol x L(-1); P =.005). Plasma cyclic guanosine monophosphate levels increased after 30 minutes of bypass in the pulsatile-flow group (25+/-18 vs. 12+/-8 pmol x mL(-1); P =.004), and urinary cyclic guanosine monophosphate excretion was higher in the pulsatile-flow group (517+/-450 vs. 118+/-78 pmol x mL(-1); P =.024). Plasma endothelin-1 levels increased in the 2 groups and were higher in the steady-flow group at 30 minutes (27+/-5 vs. 23+/-2 pg x mL(-1); P =.04) and 60 minutes of bypass (39+/-7 vs 32 +/- 6 pg x mL(-1); P =.04). Plasma renin concentration increased significantly during bypass only in the steady-flow group (26+/-10 vs. 57+/-42 in ng A1 x mL(-1) x h(-1); P =.04).
  
  
  CONCLUSIONS
  Improved placental and peripheral perfusion during fetal pulsatile-flow bypass may be mediated by preservation of fetal/maternal endothelial nitric oxide biosynthetic mechanisms and/or decreased activation of the fetal renin-angiotensin pathway.
authors.affiliation: Department of Anesthesia and Intensive Care Medicine in Cardiovascular Surgery, Louis Pradel Cardiologic Hospital, Lyon, France. vedrin@univ-lyon1.fr
authors.forename: C
authors.initials: C
authors.lastname: Vedrinne
authors.forename: F
authors.initials: F
authors.lastname: Tronc
authors.forename: S
authors.initials: S
authors.lastname: Martinot
authors.forename: J
authors.initials: J
authors.lastname: Robin
authors.forename: A M
authors.initials: AM
authors.lastname: Allevard
authors.forename: M
authors.initials: M
authors.lastname: Vincent
authors.forename: J J
authors.initials: JJ
authors.lastname: Lehot
authors.forename: M
authors.initials: M
authors.lastname: Franck
authors.forename: G
authors.initials: G
authors.lastname: Champsaur
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D002315:Cardiopulmonary Bypass; D005260:Female; D005333:Fetus / Q000601:surgery*; D006439:Hemodynamics / Q000502:physiology*; D000860:Hypoxia / Q000517:prevention & control; D021041:Placental Circulation / Q000502:physiology; D011247:Pregnancy; D011673:Pulsatile Flow / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000502:physiology*; D012756:Sheep; D014655:Vascular Resistance / Q000502:physiology; D014665:Vasodilator Agents / Q000378:metabolism
chemical_list: D014665:Vasodilator Agents