Better preservation of endothelial function and decreased activation of the fetal renin-angiotensin pathway with the use of pulsatile flow during experimental fetal bypass.
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.
Vedrinne
C
C
Department of Anesthesia and Intensive Care Medicine in Cardiovascular Surgery, Louis Pradel Cardiologic Hospital, Lyon, France. vedrin@univ-lyon1.fr
Tronc
F
F
Martinot
S
S
Robin
J
J
Allevard
A M
AM
Vincent
M
M
Lehot
J J
JJ
Franck
M
M
Champsaur
G
G
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
D014665:Vasodilator Agents