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 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% 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 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.