Prostanoid production in the umbilicoplacental arterial tree relative to impaired glucose tolerance.
The purpose of this study was to investigate prostanoid synthesis in different segments of the umbilicoplacental vascular tree and its relationship to impaired maternal glucose tolerance. Segments from the umbilical artery and vein, allantochorionic artery branches, and the cotyledon artery from 21 women with diabetes or impaired glucose tolerance and 10 healthy women were studied. Production of prostacyclin (PGI2) and thromboxane (TxA2) metabolites was determined. The Mann-Whitney U test, Wilcoxon signed-ranks matched-pairs test, Kruskal-Wallis test, analysis of variance, and simple linear regression analysis were used. A two-tailed P value of < 0.05 was considered statistically significant. From the umbilical artery distal to the cotyledon artery, the PGI2 synthesis decreased and the TxA2 synthesis increased gradually towards the periphery in normal pregnancy. The PGI2/TxA2 ratio was more than 200 times higher in the umbilical artery than in the cotyledon artery. The TxA2 production tended in general to be higher in the diabetic group than in the control group, resulting in significantly lower PGI2/TxA2 ratios in some vessels. The prostanoid production was not significantly correlated to maternal HbA1c or cord C-peptide concentrations. The balance between vascular prostacyclin and thromboxane synthesis in the umbilicoplacental arterial tree changed gradually towards the periphery: the more peripheral, the lower the prostacyclin and the higher the thromboxane production. The physiological role of this phenomenon is unknown, but may be of importance for the equilibration of vascular tone between arteries of different calibers. The altered prostanoid balance found in diabetic pregnancy was not directly attributable to the degree of maternal glycemic control, but may reflect increased free radical activity and peroxide production in diabetes.
Saldeen
P
P
Department of Obstetrics and Gynecology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia.
Olofsson
P
P
Parhar
R S
RS
al-Sedairy
S
S
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis*; D015331:Cohort Studies; D046508:Culture Techniques; D003924:Diabetes Mellitus, Type 2 / Q000196:embryology* / Q000378:metabolism; D016640:Diabetes, Gestational / Q000196:embryology* / Q000378:metabolism; D005260:Female; D018149:Glucose Intolerance / Q000196:embryology* / Q000378:metabolism; D005951:Glucose Tolerance Test; D006801:Humans; D010920:Placenta / Q000098:blood supply*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D012016:Reference Values; D013928:Thromboxane A2 / Q000096:biosynthesis*; D014469:Umbilical Arteries / Q000033:anatomy & histology / Q000166:cytology / Q000378:metabolism*
D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha