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

Autor: Alfons C. Wouterse, Paul Smits, L.D. Elving, Frans G. M. Russel, Eric A.P. Steegers, Tanya M. Bisseling
Přispěvatelé: Obstetrics & Gynecology
Rok vydání: 2005
Předmět:
Adult
medicine.medical_specialty
Endothelium
Endocrinology
Diabetes and Metabolism
Indomethacin
Pregnancy in Diabetics
Membrane transport and intracellular motility [NCMLS 5]
Blood Pressure
Vasodilation
Vascular medicine and diabetes [UMCN 2.2]
In Vitro Techniques
Endocrinology
SDG 3 - Good Health and Well-being
Indometacin
Pregnancy
Internal medicine
Diabetes mellitus
Internal Medicine
medicine
Humans
Cyclooxygenase Inhibitors
Placental Circulation
Renal disorder [IGMD 9]
Type 1 diabetes
Cardiovascular diseases [NCEBP 14]
biology
Endocrinology and reproduction [UMCN 5.2]
business.industry
Effective Hospital Care [EBP 2]
medicine.disease
Renal disorders [UMCN 5.4]
Diabetes Mellitus
Type 1
Blood pressure
medicine.anatomical_structure
Prostaglandin-Endoperoxide Synthases
Vasoconstriction
Enzyme inhibitor
biology.protein
Female
Cyclo-oxygenase
business
Signal Transduction
medicine.drug
Zdroj: Diabetic Medicine, 22(4), 503-506. Wiley-Blackwell Publishing Ltd
Diabetic Medicine, 22, 503-6
Diabetic Medicine, 22, 4, pp. 503-6
ISSN: 1464-5491
0742-3071
DOI: 10.1111/j.1464-5491.2005.01437.x
Popis: Contains fulltext : 48788.pdf (Publisher’s version ) (Closed access) AIM: 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. METHODS: We performed ex-vivo perfusions 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. RESULTS: 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). CONCLUSIONS: 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.
Databáze: OpenAIRE
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