Alterations in relaxation to lactate and H2O2in human placental vessels from gestational diabetic pregnancies

2000 ◽  
Vol 278 (3) ◽  
pp. H706-H713 ◽  
Author(s):  
Reinaldo Figueroa ◽  
Edilberto Martinez ◽  
Raisa P. Fayngersh ◽  
Nergesh Tejani ◽  
Kamal M. Mohazzab-H. ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Arachidonic Acid ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Contractile Response ◽  
Full Term ◽  
Nitrite Production ◽  
Prostaglandin F ◽  
Arteries And Veins

We determined whether alterations in the mechanism of relaxation to H2O2potentially contribute to the enhanced prostaglandin-mediated contractile response to H2O2and posthypoxic reoxygenation seen in human placental vessels of pregnancies with gestational diabetes mellitus (GDM). Isolated placental arteries and veins from GDM and uncomplicated full-term pregnancies were precontracted with prostaglandin F2α([Formula: see text] 35–38 Torr) and then exposed to lactate (1–10 mM), arachidonic acid (0.01–10 μM), nitroglycerin (1 nM–1 μM), forskolin (0.01–10 μM), or H2O2(1 μM–1 mM + 10 μM indomethacin). The rates of tissue H2O2metabolism by catalase and nitrite production were measured. The relaxation to lactate was reduced in GDM placental arteries and veins by 54–85 and 66–80%, and the relaxation to H2O2was inhibited by 80–94% in GDM placental veins compared with vessels from uncomplicated full-term pregnancies. H2O2caused only minimal relaxation of placental arteries. Responses to other relaxing agents were not altered in the GDM placental vessels. Diabetic vessels showed rates of nitrite production that were increased by 113–195% and rates of H2O2metabolism by catalase that were decreased by 44–61%. The loss of relaxation to H2O2and lactate (mediated via H2O2), perhaps as a result of the inhibition of catalase by nitric oxide, may explain the previously reported enhancement of prostaglandin-mediated contractile responses to H2O2and posthypoxic reoxygenation seen in GDM placental vessels.

scholarly journals Fetoplacental Vascular Endothelial Dysfunction as an Early Phenomenon in the Programming of Human Adult Diseases in Subjects Born from Gestational Diabetes Mellitus or Obesity in Pregnancy

2011 ◽  
Vol 2011 ◽  
pp. 1-18 ◽  
Author(s):  
Andrea Leiva ◽  
Fabián Pardo ◽  
Marco A. Ramírez ◽  
Marcelo Farías ◽  
Paola Casanello ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Convincing Evidence ◽  
Amino Acid Transporters ◽  
Pathological State ◽  
Metabolic Marker ◽  
Obesity In Pregnancy ◽  
In Pregnancy

Gestational diabetes mellitus (GDM) and obesity in pregnancy (OP) are pathological conditions associated with placenta vascular dysfunction coursing with metabolic changes at the fetoplacental microvascular and macrovascular endothelium. These alterations are seen as abnormal expression and activity of the cationic amino acid transporters and endothelial nitric oxide synthase isoform, that is, the “endothelial L-arginine/nitric oxide signalling pathway.” Several studies suggest that the endogenous nucleoside adenosine along with insulin, and potentially arginases, are factors involved in GDM-, but much less information regards their role in OP-associated placental vascular alterations. There is convincing evidence that GDM and OP prone placental endothelium to an “altered metabolic state” leading to fetal programming evidenced at birth, a phenomenon associated with future development of chronic diseases. In this paper it is suggested that this pathological state could be considered as a metabolic marker that could predict occurrence of diseases in adulthood, such as cardiovascular disease, obesity, diabetes mellitus (including gestational diabetes), and metabolic syndrome.

scholarly journals Mitochondrial content, oxidative, and nitrosative stress in human full-term placentas with gestational diabetes mellitus

2017 ◽  
Vol 15 (1) ◽  
Author(s):  
Joel Ramírez-Emiliano ◽  
Martha E. Fajardo-Araujo ◽  
Ismael Zúñiga-Trujillo ◽  
Victoriano Pérez-Vázquez ◽  
Cuauhtémoc Sandoval-Salazar ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Nitrosative Stress ◽  
Full Term ◽  
Mitochondrial Content ◽  
Oxidative And Nitrosative Stress

Gestational diabetes mellitus was related to ambient air pollutant nitric oxide during early gestation

2017 ◽  
Vol 158 ◽  
pp. 318-323 ◽  
Author(s):  
Shih-Chun Pan ◽  
Ching-Chun Huang ◽  
Shio-Jean Lin ◽  
Bing-Yu Chen ◽  
Chang-Chuan Chan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Ambient Air ◽  
Air Pollutant ◽  
Early Gestation

scholarly journals Impaired vasocontractile responses to adenosine in chorionic vessels of human term placenta from pregnant women with pre-existing and gestational diabetes

2018 ◽  
Vol 15 (6) ◽  
pp. 528-540 ◽  
Author(s):  
Azlina A Razak ◽  
Lopa Leach ◽  
Vera Ralevic
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Type 1 Diabetes Mellitus ◽  
Isometric Tension ◽  
Receptor Protein ◽  
Protein Levels ◽  
Arteries And Veins

Background: There is clinical and experimental evidence for altered adenosine signalling in the fetoplacental circulation in pregnancies complicated by diabetes, leading to adenosine accumulation in the placenta. However, the consequence for fetoplacental vasocontractility is unclear. This study examined contractility to adenosine of chorionic vessels from type 1 diabetes mellitus, gestational diabetes mellitus and normal pregnancies. Methods: Chorionic arteries and veins were isolated from human placenta from normal, gestational diabetes mellitus and type 1 diabetes mellitus pregnancies. Isometric tension recording measured responses to adenosine and the thromboxane A2 analogue U46619 (thromboxane A2 mediates fetoplacental vasoconstriction to adenosine). Adenosine and thromboxane prostanoid receptor protein expression was determined by immunoblotting. Results: Adenosine elicited contractions in chorionic arteries and veins which were impaired in both gestational diabetes mellitus and type 1 diabetes mellitus. Contractions to potassium chloride were unchanged. Adenosine A2A and A2B receptor protein levels were not different in gestational diabetes mellitus and normal pregnancies. Contractions to U46619 were unaltered in gestational diabetes mellitus arteries and increased in type 1 diabetes mellitus arteries. Overnight storage of vessels restored contractility to adenosine in gestational diabetes mellitus arteries and normalized contraction to U46619 in type 1 diabetes mellitus arteries. Conclusion: These data are consistent with the concept of aberrant adenosine signalling in diabetes; they show for the first time that this involves impaired adenosine contractility of the fetoplacental vasculature.

scholarly journals Clinical, metabolic and neurological disorders in full-term newborns from mothers with gestational diabetes mellitus

2021 ◽  
Vol 66 (3) ◽  
pp. 46-51
Author(s):  
O. V. Remneva ◽  
O. V. Rozhkova ◽  
T. M. Cherkasova ◽  
Yu. V. Korenovskiy ◽  
N. V. Trukhacheva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Full Term ◽  
Electrolyte Balance ◽  
Maternal Hyperglycemia ◽  
The Central Nervous System ◽  
Postnatal Adaptation

Objective. To determine the clinical and metabolic changes in children born from mothers with gestational diabetes mellitus and to predict perinatal injury of the central nervous system (CNS), taking into account the level of maternal hyperglycemia.Material and methods. The period of early postnatal adaptation was analyzed in 258 full-term infants, who were divided into two groups, depending on the glucose level in the mother’s venous blood during pregnancy: Group 1: 5,1–5,6 mmol/L, Group 2: 5,7–7,0 mmol/L.Results. Based on clinical, functional and laboratory markers (electrolyte balance and carbohydrate metabolism in the blood of a newborn) there was established a correlation between the severity of maternal hyperglycemia and the severity of neonatal disorders. In Group II infants born from mothers with more severe hyperglycemia are more likely to have a respiratory distress syndrome and ischemic-hypoxic injury of the central nervous system in combination with excess birth weight which significantly complicates postnatal adaptation.Conclusion. The concentration of neuron-specific enolase of 4,9 ng/ml in the fetal amniotic fluid is an antenatal marker of perinatal damage to the central nervous system in a newborn.

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