Objective To evaluate the role of reduced fetal oxygen supply on morphological impairment in aorta from the adult offspring and further assess its susceptibility to sex-, hyperlipidaemia-, and postnatal hypoxaemia-related differences.
Methods Based on a 4×2 full factorial design consisting of four factors (maternal hypoxia, sex, hyperlipidaemia, and postnatal hypoxaemia), pregnant Sprague-Dawley rats were subjected to hypoxia for 3 h in a low pressure cabin with an oxygen concentration of 10%±1% from (for) 7 to 21 days of gestation and their offsprings were subjected to high-fat diet feeding (at 10 months of age for 4 months) or hypoxia (at 12 months of age for 4 weeks). The histopathological observation and morphometric analysis of the thoracic aortas were performed in (on a) rat offspring at 16 months of age.
Results In a 16-mo-old maternal hypoxia offspring, the thoracic aortas exhibited lesions are similar to early events in atherosclerosis that involved impaired endothelial cells, thickening and fibration of intimas, infiltration of inflammatory cells to the subendothelial space, and migration and proliferation of vascular smooth muscle cells to the intima. In contrast, no detectable pathological changes were observed in the offspring without maternal hypoxia exposure. Morphometric analysis further demonstrated that prenatal hypoxia caused a significant thickening of intima (p<0.001) with a main effect of 5.5 μm, an approximately twofold increase compared with controls. In addition, there was a positive additive relationship between prenatal hypoxia and hyperlipidaemia on the intimal thickness (p<0.05). There were no other main effects or interaction among these four factors.
Conclusions Intrauterine chromic hypoxia can induce early pathological appearances of atherogenesis in adult offspring. This effect was enhanced with hyperlipaemia but was unaffected by postnatal hypoxia or sex.
- Intrauterine chronic hypoxia
- morphological impairment
- maternal hypoxia
- and postnatal hypoxaemia
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