SHEAR-STRESS MAY STIMULATE RELEASE AND ACTION OF NITRIC-OXIDE IN THE HUMAN FETAL-PLACENTAL VASCULATURE

OBJECTIVE: Our purpose was to determine the effect of perfusate flow o r viscosity on release and action of nitric oxide in the human fetal-p lacental vasculature in vitro. STUDY DESIGN: Cotyledons from normal te rm placentas were perfused with Hanks' buffered saline solution gassed with 95% oxygen and 5% carbon dioxide, pH 7.4, at 37 degrees C with a maternal flow rate of 10 ml/min. Fetal flow rate was varied from 1 to 10 ml/min at 10-minute intervals (n = 6), and perfusion pressure was recorded. Viscosity was varied by perfusion of both circulations with Hanks' balanced salt solution containing 0, 2.5, 5.0, 7.5, or 10% dext ran, the concentration being changed every 20 minutes and pressure rec orded at fetal flow rates of 4 (n = 4) or 1 ml/min (n = 7). All experi ments were performed in the presence or absence of the nitric oxide sy nthase inhibitor N-nitro-L-arginine (10(-3) mol/L) in the same placent as. Data were analyzed by analysis of variance with repeated measures. RESULTS: Increasing fetal flow rate with or without N-nitro-L-arginin e resulted in a significant increase in perfusion pressure (p = 0.0011 ). Addition of N-nitro-L-arginine gave an overall significant increase in perfusion pressure (p = 0.0048). At a fetal flow rate of 4 ml/min increasing dextran concentration with or without N-nitro-L-arginine ga ve a significant increase in perfusion pressure (p = 0.0011), but the increase in perfusion pressure in the presence of N-nitro-L-arginine d id not reach significance (p = 0.06). At 1 ml/min increasing dextran c oncentration resulted in a significant increase in fetal perfusion pre ssure (p = 0.001), but no significant effect of N-nitro-L-arginine was observed. CONCLUSION: Altering shear stress by increasing fetal flow rate or viscosity of the medium may increase synthesis and release of nitric oxide, which attenuates increases in perfusion pressure.