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Hyperglycemia has been shown to impact the body's ability to regulate blood supply via excess uptake of endogenously produced nitric oxide. Lacking any neural stimulus, fetal-placental vascular tone is regulated via autocrine mechanisms, specifically vascular production of nitric oxide. We sought to investigate the effects of maternal hyperglycemia on the placenta's ability to self regulate its blood flow.
Using the placental perfusion model, 15 unlabored placentas at term were analyzed. Vascular responsiveness, as measured by pressure change from baseline, was recorded following serial injections of L-NAME, a nitric oxide inhibitor, into the fetal circulation. Dextrose was then added to the circulatory bath at a concentration of 8 × 10−3 M, and serial injections of L-NAME were again administered; pressure change from baseline was again recorded. The pressure changes between the normoglycemic and hyperglycemic placentas were compared at each concentration of L-NAME. The data was analyzed using the Mann-Whitney U test.
Fetal vascular responsiveness, as measured by the change in pressure, was diminished in 10/15 placentas at an L-NAME concentration of 10−3 M, 7/15 at 10−4 M, 9/14 at 10−5 M, and 6/15 at 10−6 M. There was a significant difference in the change in pressure in the normoglycemic placenta vs. the hyperglycemic placenta after injection of L-NAME at 10−5 and 10−3 concentrations.
In an in vitro placental perfusion model, placental hyperglycemia appears to reduce the nitric oxide inhibition effects of L-NAME, reaching statistical significance at 10−5 and 10−3.