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Decrease in inflammatory response does not prevent placental dysfunction after fetal cardiac bypass in goats.

Cheng-Bin Zhou1, Jian Zhuang, Ji-Mei Chen

  • 1Department of Cardiovascular Surgery, Guangdong Provincial Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.

The Journal of Thoracic and Cardiovascular Surgery
|August 9, 2011
PubMed
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Fetal cardiac bypass increases placental vascular resistance and inflammation, potentially via nuclear factor kappa-B (NF-KB). However, inhibiting NF-KB did not alleviate this placental dysfunction in a goat model.

Area of Science:

  • Cardiovascular Research
  • Reproductive Biology
  • Immunology

Background:

  • Fetal cardiac bypass can lead to severe placental dysfunction, characterized by increased vascular resistance.
  • Nuclear factor kappa-B (NF-KB) is a key regulator of inflammatory responses.

Purpose of the Study:

  • To investigate if fetal cardiac bypass activates NF-KB.
  • To determine if inhibiting NF-KB with pyrrolidine dithiocarbamate can prevent placental dysfunction.

Main Methods:

  • Pregnant goats underwent fetal cardiac bypass with or without NF-KB inhibition.
  • Placental vascular resistance, fetal plasma markers (NO, ET-1, 6-K, TXB2, IL-6, TNF-α), and NF-KB activation were measured.

Main Results:

  • Fetal bypass increased placental vascular resistance and inflammatory markers (IL-6, TNF-α).

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  • NF-KB activation was elevated in the fetal bypass group.
  • Inhibiting NF-KB did not reduce placental dysfunction or inflammation.

    • Conclusions:

    • Fetal cardiac bypass triggers an inflammatory response mediated by NF-KB, causing placental dysfunction.
    • Pharmacologic inhibition of NF-KB did not alleviate the observed placental dysfunction.