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Fetal Mouse Cardiovascular Imaging Using a High-frequency Ultrasound (30/45MHZ) System
Published on: May 5, 2018
Offspring myocardium alteration from dams submitted to nitric oxide synthesis inhibition during pregnancy
Veronica C V Martini1, Carlos A Mandarim-de-Lacerda
1Laboratory of Morphometry and Cardiovascular Morphology, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Background:
Nitric oxide synthesis (NOS) inhibition during pregnancy alters offspring cardiac structure.
Methods:
Thirty female Wistar rats were assigned to two groups: control (15 rats) and LN (15 rats). LN rats received N(omega)-nitro-L-arginine methyl ester (L-NAME) during 5 weeks (2 weeks before matching and the weeks of pregnancy). Offspring were separated and sacrificed in three age groups (n=5): 2, 15 and 30 postnatal days. Left ventricular myocardium was analyzed with light microscopy and stereology.
Results:
BP increased significantly in LN matrices. No significant difference in neonate C-R length, body mass (BM) nor heart mass (HM) occurred in control and LN groups with 2 days of life. HM was greater in LN group than in control group from 15 days of life; BM was greater in LN group than in control group only with 30 days of life. HM/BM ratio was greater in LN neonates than in control neonates in all age groups. Vasculature total length (L[VE]) increased from days 2 to 15 and from days 15 to 30 and total number of cardiomyocyte nuclei profiles (N[CM]) also increased from days 2 to 30 in both LN and control neonates.
Conclusion:
The offspring main cardiac structural alteration due to prenatal NOS inhibition is compatible with neonatal cardiac hypertrophy with intramyocardial vasculature enhancement. Furthermore, the prenatal NOS inhibition apparently stimulates the cardiomyocyte proliferation that can be observed until the end of lactation, which is when the number of cardiomyocytes nuclei profiles seems to become stable.
