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- Title
Dysfunction of the cyclo-oxygenase pathway in the foetoplacental circulation in Type 1 diabetes mellitus.
- Authors
Bisseling, T. M.; Wouterse, A. C.; Steegers, E. A. P.; Elving, L.; Russel, F. G. M.; Smits, P.
- Abstract
In diabetes, perinatal morbidity is significantly increased. This may partly be related to functional changes in the foetoplacental vascular bed. In diabetes models, a defect in the cyclo-oxygenase pathway is a common observation. Therefore, we hypothesized that the human foetoplacental circulation of diabetic patients is characterized by dysfunction of the cyclo-oxygenase pathway, as well.We performedex-vivoperfusions of isolated placental cotyledons from healthy women (n = 14) and from patients with Type 1 diabetes (n = 9). The contribution of cyclo-oxygenase products to foetoplacental vascular tone was quantified by measuring the response to the cyclo-oxygenase inhibitor indomethacin.Baseline foetoplacental arterial pressure was comparable between controls and diabetic women (mean ± sem, 21.7 ± 1.2 vs. 24.4 ± 2.0 mmHg). Maximum foetoplacental arterial pressure at highest dose of indomethacin was 32.8 ± 3.0 mmHg in controls vs. 27.3 ± 2.3 mmHg in diabetic women. The indomethacin-induced increase in pressure was reduced in diabetes (2.9 ± 0.7 vs. 11.2 ± 2.4 mmHg in controls,P = 0.01).Under baseline conditions, the net effect of all cyclo-oxygenase products in the foetoplacental vascular bed is vasodilation. In diabetes, this vasodilator effect seems significantly impaired.Diabet. Med. 22, 503–506 (2005)
- Subjects
OXYGENASES; DIABETES; ENDOCRINE diseases; PEOPLE with diabetes; VASCULAR diseases; NONSTEROIDAL anti-inflammatory agents
- Publication
Diabetic Medicine, 2005, Vol 22, Issue 4, p503
- ISSN
0742-3071
- Publication type
Article
- DOI
10.1111/j.1464-5491.2005.01437.x