Signs of platelet activation, but not lipid peroxidation, in fetal blood associated with functional and structural umbilicoplacental lesions in pregnancies complicated by impaired glucose metabolism.
OBJECTIVE
To study the influence of platelet activation and lipid peroxidation in fetal blood on umbilical vascular prostanoid synthesis and placental morphology in diabetic pregnancy.


METHODS
The concentrations of thromboxane A2 (TxA2) and malondialdehyde (MDA) were determined in umbilical cord plasma in 21 women with diabetes mellitus/impaired glucose tolerance (DM/IGT) and ten healthy women. Segments from the umbilical artery and vein were incubated and prostacyclin (PGI2) and TxA2 metabolites were determined. Prostanoid synthesis was stimulated with calcium ionophore at a second incubation. Histological examination was carried out in samples from the umbilical cord, membranes and placental parenchyma. Non-parametric statistical analysis was used, with a two-tailed p < 0.05 considered statistically significant.


RESULTS
Cord plasma TxA2, but not MDA, was higher among DM/IGT women (p = 0.07). There were indications that cord plasma TxA2, but not MDA, was positively correlated with vascular prostanoid synthesis and synthesis capacity. In the umbilical vein, both the basal and stimulated PGI2 production and the stimulated TxA2 production were lower in the DM/IGT group. Ischemic placental lesions were associated with a high TxA, and a low MDA concentration in cord plasma.


CONCLUSIONS
Even in less severe forms of impaired glucose metabolism, disturbances in platelet activation significantly affect both biochemical and morphological vessel wall and tissue functions in the umbilicoplacental unit. This could indicate an abnormal programming of fetal cell functions and designate cases at increased risk of developing cellular and organ damage.
Saldeen
P
P
Department of Obstetrics and Gynecology, Malmö University Hospital, Lund University, Malmö, Sweden.
Olofsson
P
P
Laurini
R N
RN
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D002096:C-Peptide / Q000097:blood; D005314:Embryonic and Fetal Development; D011464:Epoprostenol / Q000378:metabolism; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D018149:Glucose Intolerance / Q000378:metabolism*; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D015227:Lipid Peroxidation; D008315:Malondialdehyde / Q000097:blood; D010920:Placenta / Q000098:blood supply / Q000473:pathology; D010922:Placenta Diseases / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D015539:Platelet Activation; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism*; D013928:Thromboxane A2 / Q000097:blood / Q000378:metabolism; D013929:Thromboxane B2 / Q000096:biosynthesis / Q000097:blood; D014469:Umbilical Arteries / Q000378:metabolism; D014471:Umbilical Veins / Q000378:metabolism
D015121:6-Ketoprostaglandin F1 alpha; D002096:C-Peptide; D011464:Epoprostenol; D006442:Glycated Hemoglobin; D008315:Malondialdehyde; D013928:Thromboxane A2; D013929:Thromboxane B2