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 or viscosity on release and action of nitric oxide in the human fetal-placental vasculature in vitro. STUDY DESIGN: Cotyledons from normal term placentas were perfused with Hanks' buffered saline solution gassed with 95% oxygen and 5% carbon dioxide, pH 7.4, at 37° 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% dextran, the concentration being changed every 20 minutes and pressure recorded at fetal flow rates of 4 (n = 4) or 1 ml/min (n = 7). All experiments were performed in the presence or absence of the nitric oxide synthase inhibitor N-nitro-l-arginine (10^-3 mol/L) in the same placentas. Data were analyzed by analysis of variance with repeated measures. RESULTS: Increasing fetal flow rate with or without N-nitro-l-arginine 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 gave a significant increase in perfusion pressure (p = 0.0011), but the increase in perfusion pressure in the presence of N-nitro-l-arginine did not reach significance (p = 0.06). At 1 ml/min increasing dextran concentration resulted in a significant increase in fetal perfusion pressure (p = 0.001), but no significant effect on 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 perfusino pressure.