Impact of Maternal Inflammation and Neonatal Hyperoxia on Heart Development in Mice
Author Information
Author(s): Velten Markus, Hutchinson Kirk R., Gorr Matthew W., Wold Loren E., Lucchesi Pamela A., Rogers Lynette K.
Primary Institution: The Research Institute at Nationwide Children's Hospital, The Ohio State University
Hypothesis
Systemic maternal inflammation and neonatal hyperoxia exposure compromise cardiac structure, resulting in LV dysfunction during adulthood.
Conclusion
Systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood.
Supporting Evidence
- Echocardiography revealed persistent lower left ventricular fractional shortening in LPS/O2 mice.
- Isolated cardiomyocytes from LPS/O2 mice had slower rates of contraction and relaxation.
- Capillary density was lower in LPS/O2 mice at 8 weeks of life.
Takeaway
Mice exposed to inflammation during pregnancy and high oxygen after birth had heart problems later in life, showing that early life conditions can affect health as adults.
Methodology
Pregnant mice were injected with LPS or saline, and offspring were exposed to room air or hyperoxia; cardiac function was assessed using echocardiography and molecular analyses.
Limitations
The study was conducted in a mouse model, which may not fully replicate human conditions.
Participant Demographics
C3H/HeN mice, both male and female.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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