Oxidative damage and nitric oxide synthase induction by surgical uteroplacental circulation restriction in the rabbit fetal heart
| Autor: | Jocelyn Rocco, Eduard Gratacós, Sebastian E. Illanes, Elisenda Eixarch, Claudia Cabezas, H. Figueroa, Edgar Hernandez-Andrade, Cristobal Alvarado, Jorge Cifuentes, Mauricio Lozano, Carlos E. Irarrazabal |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty H&E stain Intrauterine growth restriction medicine.disease_cause Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Enos Internal medicine medicine Genetics (clinical) Fetus 030219 obstetrics & reproductive medicine biology Obstetrics and Gynecology medicine.disease biology.organism_classification Nitric oxide synthase 030104 developmental biology Endocrinology chemistry Uteroplacental Circulation biology.protein Oxidative stress |
| Zdroj: | Prenatal Diagnosis. 37:453-459 |
| ISSN: | 0197-3851 |
| Popis: | Objective This study investigated the role of oxidative damage and nitric oxide (NO) synthases in the fetal heart using a model of intrauterine growth restriction (IUGR) induced by uteroplacental circulation restriction (UCR). Methods New Zealand white rabbits kept under 12 hr light cycles, with food and water provided ad libitum, were subjected at day 25 of pregnancy to 40%-50% uteroplacental artery ligation. We analyzed the gene expression of enzymes linked to nitric oxide synthesis (iNOS, eNOS, HO-1, and ARG-2), HIF-1α and the state of oxidative stress (protein carbonyl levels) in fetal heart homogenates. Additionally, we studied the histological morphology of the fetal heart. Results We found that fetal growth restriction was associated with a significant reduction in heart weight but a normal heart/body weight ratio in UCR animals. Hematoxylin and eosin staining showed normal left and right ventricular thickness but increased vessel dilatation with hyperemia in hearts from the UCR group. We observed HIF-1α, eNOS, p-eNOS, and iNOS induction concomitant with intensified protein carbonyl levels but observed no changes in HO-1 or Arg-2 expression, suggesting increased NO and oxidative stress in the hearts of UCR animals. Conclusion UCR increased NO-linked enzymes, oxidative damage and dilated coronary vessels in fetal hearts. |
| Databáze: | OpenAIRE |
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