No abstract

No abstract

In the dual perfused, single isolated cotyledon, human placental model, exposure of the maternal circulation to ephedrine and phenylephrine caused an increase in FAP, whereas exposure to norepinephrine, epinephrine, and methoxamine did not. The pharmacodynamic mechanisms underlying these differences have yet to be explained. Thus, the clinical implications of the findings are as yet unclear.

We investigated the characteristics of hypoxemic fetoplacental vasoconstriction (HFPV) in the dual perfused, single isolated human placental cotyledon. Fetal arterial blood pressures (FAP) were measured in four cotyledons (Group 1) equilibrated with 21% oxygen (O2), 5% carbon dioxide (CO2), and nitrogen (N2) [control] followed by 5% CO2 in N2 for 30 min. FAP (mean +/- sd) increased from 69.8 (+/- 6.4) to 105 (+/- 3.0) mm Hg (P < 0.05), confirming the utility of HFPV in the human placenta. Eight more cotyledons (Group 2) were exposed sequentially and alternately at 15-min intervals to the control gases and to gas blends containing 15%, 12%, 5%, and 0% O2 with 5% CO2 and N2. FAP increased significantly (P < 0.05) in a stepwise fashion from 68.7 (+/- 3.7) to 70.5 (+/- 3.3) mm Hg with 15% O2; from 69.3 (+/- 3.8) to 72.4 (+/- 4.3) mm Hg with 12% O2; from 67.8 (+/- 3.2) to 74.5 (+/- 3.4) mm Hg with 5% O2; and from 69.7 (+/- 3.4) to 77.9 (+/- 5.9) mm Hg with 0% O2, suggesting that HFPV is a graduated response to reduced O2 conditions in the human placenta.