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Updated: Jul 6, 2026
A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
Increased elastic tissue defect formation in the growth restricted Brown Norway rat: a potential link between in
Katie C Pascoe1, Mary E Wlodek, Gregory T Jones
1Department of Surgery, University of Otago, Dunedin, New Zealand.
Insights
Low birth weight in newborns, caused by in utero growth restriction, significantly increases aortic internal elastic lamina (IEL) defects in adult rats. This finding supports the fetal origins of adult disease hypothesis, independent of blood pressure.
Area of Science:
- Cardiovascular Science
- Developmental Biology
- Pathology
Background:
- Low birth weight for gestational age is linked to adult cardiovascular disease.
- Aortic internal elastic lamina (IEL) disruption is an early sign of atherosclerosis.
- The impact of in utero growth restriction on early atherosclerotic markers is not fully understood.
Purpose of the Study:
- To investigate if in utero growth restriction affects aortic IEL integrity in adult rats.
- To determine the relationship between fetal growth restriction and early atherosclerotic pathology.
Main Methods:
- In utero growth restriction was induced in Brown Norway (BN) rats via bilateral uterine artery ligation on day 18 of gestation.
- Newborn pup weight was reduced by approximately 14% to model growth restriction.
- Aortic IEL defect numbers were quantified at 8 and 16 weeks of age in control and growth-restricted groups.
Main Results:
- Growth restriction significantly increased aortic IEL defect numbers in both sexes at 8 weeks.
- At 16 weeks, males from the restriction group showed significantly more IEL defects than controls.
- IEL defect numbers correlated with postnatal growth parameters but not with blood pressure.
Conclusions:
- Moderate in utero growth restriction significantly increases aortic elastic tissue defects in adult rats.
- These findings support the fetal origins of adult disease hypothesis.
- The observed increase in IEL defects occurs independently of significant changes in blood pressure.
Abstract:
Low birth weight for gestational age has been epidemiologically linked to cardiovascular mortality and morbidity in adult life. This study aimed to determine whether in utero growth restriction influences an early feature of atherosclerotic pathology; disruption of the aortic internal elastic lamina (IEL) in the adult Brown Norway (BN) rat. In utero growth restriction was induced by bilateral uterine artery ligation on day 18 of gestation, thereby decreasing newborn BN pup weight by approximately 14%. Restriction surgery significantly increased aortic IEL defect number at 8 wk of age in both sexes compared with no surgery animals (p < 0.002). At 16 wk of age placental restriction surgery significantly increased the number of defects in males compared with both no surgery and sham surgery control groups (p < 0.001). The total number of IEL defects was significantly correlated with several postnatal growth rate parameters, including 72-h postpartum weight. Neither blood pressure was significantly different between treatment groups, nor was it correlated with body weight or IEL defect numbers. The findings of this study seem to support the fetal origins of adult disease hypothesis, by demonstrating that a moderate growth restricting insult dramatically increases aortic elastic tissue defect formation via an apparently blood pressure-independent mechanism.
