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Dysfunction of the cyclo-oxygenase pathway in the foetoplacental circulation in Type 1 diabetes mellitus

T M Bisseling1, A C Wouterse, E A P Steegers

  • 1Department of Pharmacology-Toxicology, University Medical Cenger, Nijmegen, the Netherlands.

Diabetic Medicine : a Journal of the British Diabetic Association
|March 25, 2005
PubMed

Insights

Diabetic pregnancies show impaired cyclo-oxygenase pathway function in the foetoplacental circulation. This dysfunction reduces the normal vasodilator effect of cyclo-oxygenase products, impacting fetal well-being.

Area of Science:

  • Reproductive Medicine
  • Vascular Biology
  • Endocrinology

Background:

  • Diabetes mellitus significantly increases perinatal morbidity.
  • Functional changes in the fetoplacental vascular bed may contribute to this increased risk.
  • Defects in the cyclo-oxygenase pathway are frequently observed in diabetes models.

Purpose of the Study:

  • To investigate the hypothesis that the human fetoplacental circulation in diabetic patients exhibits cyclo-oxygenase pathway dysfunction.
  • To quantify the contribution of cyclo-oxygenase products to fetoplacental vascular tone in diabetic versus healthy pregnancies.

Main Methods:

  • Ex-vivo perfusion of isolated placental cotyledons from women with Type 1 diabetes (n=9) and healthy controls (n=14).
  • Measurement of fetoplacental arterial pressure responses to the cyclo-oxygenase inhibitor indomethacin to assess pathway activity.

Main Results:

  • Baseline fetoplacental arterial pressure was similar between control and diabetic groups.
  • The increase in arterial pressure induced by indomethacin was significantly reduced in diabetic placentas compared to controls (2.9 mmHg vs. 11.2 mmHg, P=0.01).

Conclusions:

  • Cyclo-oxygenase products normally exert a vasodilatory effect in the fetoplacental vascular bed.
  • This vasodilatory effect appears significantly impaired in pregnancies complicated by diabetes.
Abstract

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