COVID-19 infection during pregnancy is associated with an increased incidence of preterm birth but neonatal infection is rare. We assessed pathways by which SARS-CoV-2 could access the placenta and contribute to fetal transmission. Placentas from pregnancies complicated with chorioamnionitis (ChA), exhibited increased expression of ACE2 mRNA. Treatment of 2nd trimester placental explants with LPS, induced an acute increase in cytokine expression followed by ACE2 mRNA. Placental ACE2 protein localized to syncytiotrophoblast, in fetal blood vessels and M1/M2 macrophage and neutrophils within the villous stroma. Increased numbers of M1 macrophage and neutrophils were present in the placenta of ChA pregnancies. Maternal peripheral immune cells (mainly granulocytes and monocytes) express the ACE2 mRNA and protein. These data suggest that in COVID19 positive pregnancies complicated by ChA, ACE2 positive immune cells have the potential to traffic SARS-CoV-2 virus to the placenta and increase the risk of vertical transmission to the placenta/fetus.
Reduction in concentration of prostaglandins in plasma by administration of sodium meclofenamate to pregnant sheep failed to alter the frequency or duration of electromyographic activity bursts or the response to oxytocin of myometrial tissue transplanted to the omentum. However, a significant (P < 0.05) delay (8.6 +/- 3.8 versus 1.3 +/- 0.3 min) in the myometrial response to oxytocin was observed when the hormone was administered 1 min after a spontaneous burst of electromyographic activity compared with 15 min after a burst, indicating a period of refractoriness. Similarly, the myometrial threshold for electrical stimulation was higher at 10-25% of the interval between contractions than close to the expected time of the next contraction. Stimulation of the myometrium at intervals of 30 s revealed a cycling of the electrical stimulation threshold: significantly higher voltages were required to elicit responses between spontaneous bursts of electromyographic activity (18.0 +/- 2.2 V) than during bursts (11.3 +/- 1.6 V). In contrast, there was no voltage differential in animals close to labour (< 24 h). These data provide no evidence to support a role for prostaglandins in the generation of contractions during pregnancy, but suggest that periodicity of contractions is associated with inherent changes in myometrial responsiveness to stimulation, which could occur as a result of a cycling of the resting membrane potential.
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