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Hydrogen sulfide in high concentrations vasodilates the fetoplacental circulation in the dual-perfused, single isolated human placental cotyledon.
Abstract Number: F 34
Abstract Type: Original Research
Introduction: Hydrogen sulfide (H2S), a new endogenous gasotransmitter produced in vascular endothelium from homocysteine, regulates human vascular tone(1). H2S is present in the placenta and corpus cavernosum(2,3). Sodium sulfide (Na2S) in solution produces H2S and HS- to generate biphasic vascular changes in non-pregnant rodent aortas(4). Lower concentrations (10 – 100 uM) constrict, higher concentrations (100 – 1600 uM) relax vasculature. H2S is intricately involved in pulmonary hypoxic vasoconstriction (PHV)(5). Hypoxemic fetoplacental vasoconstriction (HFPV) is analogous to PHV. We investigated the influence of H2S on the fetoplacental circulation.
Methods: With IRB approval and informed written consent fresh placentae (n = 5) were harvested at elective CS from healthy women at term. Organs were transported expediently to our laboratory where a fetal chorionic artery and vein serving a discrete cotyledon were isolated and cannulated. Three needles were inserted into the maternal placental interface. Both sides of the placenta were perfused with Krebs Ringers buffer (KRB) at constant pH (7.4) and temperature (37ᵒC). The open (non-recirculating) model was employed. Cotyledons were perfused for an hour to stabilize pressures. Fetal perfusion rates were held constant. With constant flow, fetal arteriolar perfusion pressures (FAP) is inversely related to arteriolar vascular resistance. FAP were recorded every 5 minutes. Na2S was added to the fetal reservoir and concentrations increased incrementally every 30 minutes (10, 30, 100, 300 uM). Thereafter 5-hydroxytryptamine (5HT) was infused demonstrating normal fetoplacental vasoconstriction. FAP recorded just before every step interval was used for data analysis. One way analysis of variance compared FAPs.
Results: FAP (α FVR) was unaffected by low Na2S concentrations (10- 100 uM) but decreased significantly over time with a high concentration (300 uM) (Figure 1).
Discussion: High concentration H2S only dilated but did not constrict the fetoplacental circulation (1). Since H2S mediates PHV, experiments utilizing H2S generators and inhibitors are needed to determine how H2S affects human HFPV in vitro.
1.Liu et al J Cardiovasc Pharmacol 2011;58:560.
2.Holwerda et al Placenta 2012; 33:518.
3.Di Villa Bianca et al PNAS 2009;106:4513.
4.Lim et al Am J Physiol Cell Physiol 2008;295:C1261.
5.Skovgaard et al Am J Physiol 2012;303:R487.