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Fetal Mouse Cardiovascular Imaging Using a High-frequency Ultrasound (30/45MHZ) System
Published on: May 5, 2018
Flow-mediated vasodilation is impaired in adult rat offspring exposed to prenatal hypoxia
J S Morton1, C F Rueda-Clausen, S T Davidge
1Dept. of Obstetrics/Gynaecology and Physiology, Univ. of Alberta, Edmonton, Alberta, Canada.
Insights
Intrauterine growth restriction (IUGR) impairs blood vessel function in aging rats, increasing cardiovascular disease risk. This study reveals altered vasodilation mechanisms in IUGR offspring, impacting long-term vascular health.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Aging Research
Background:
- Low birth weight is linked to increased mortality and cardiovascular disease risk.
- Aging exacerbates vascular endothelial dysfunction.
- The impact of intrauterine growth restriction (IUGR) on aging vascular mechanisms is not fully understood.
Purpose of the Study:
- To investigate if IUGR alters vascular function and flow-induced vasodilation mechanisms in aging rats.
- To determine if these changes are age- or sex-dependent.
Main Methods:
- An IUGR rat model was created using maternal hypoxia during pregnancy.
- Vascular function was assessed in mesenteric arteries of offspring at young (4 months) and aging (12 months) stages.
- Flow-induced vasodilation and underlying vasodilator pathways (nitric oxide, endothelium-derived hyperpolarizing factor) were analyzed.
Main Results:
- Flow-induced vasodilation was reduced in aging IUGR rats compared to controls.
- Nitric oxide-mediated vasodilation was abolished in both young and aging IUGR rats and aging control females.
- Endothelium-derived hyperpolarizing factor-mediated vasodilation remained intact across all groups.
Conclusions:
- IUGR leads to altered vasodilator mechanisms, specifically abolished nitric oxide function, by aging.
- These early-life programming changes may predispose IUGR offspring to cardiovascular disease later in life.
- Understanding these mechanisms is crucial for preventing age-related vascular dysfunction in individuals with IUGR history.
Abstract:
There is now a demonstrated association between low birth weight and increased mortality later in life. Changes in fetal development may program the cardiovascular system and lead to an increased risk of cardiovascular diseases later in life. In addition, aging is a risk factor for vascular endothelial-dependent dysfunction. However, the impact of being born intrauterine growth restricted (IUGR) on the normal aging mechanisms of vascular dysfunction is not clear. We hypothesized that IUGR would cause changes in vascular function that would affect the mechanisms of flow-induced vasodilation later in life in an age- or sex-dependent manner. To create an IUGR model, pregnant Sprague-Dawley rats were placed in a hypoxic (11.5% O₂) or control (room air, 21% O₂) environment from days 15 to 21 of pregnancy. Both male and female offspring were investigated at 4 or 12 mo of age. Vascular function was assessed in small mesenteric arteries using flow-induced vasodilation, a physiological stimuli of vasodilation, in a pressure myograph. Flow-induced vasodilation was unaffected at a young age, but was significantly reduced in aging IUGR compared with aging controls (P < 0.05). Underlying vasodilator mechanisms were altered such that nitric oxide-mediated vasodilation was abolished in both young adult and aging IUGR males and females and in aging control females (P > 0.05). Endothelium-derived hyperpolarizing factor-mediated vasodilation was maintained in all groups (P < 0.01). A change in the mechanisms of vasodilation occurring at an earlier age in IUGR offspring may predispose them to develop cardiovascular diseases as an aging adult.
