A Model of Intrauterine Growth Restriction Was Induced by Bilateral Uterine Vessel Clamping in Pregnant Rats

Author(s):  
Min Diao ◽  
Hao Li ◽  
Yi Qu ◽  
Hui Liu ◽  
Yu-Shan Ma ◽  
...  
2014 ◽  
Vol 12 (1) ◽  
pp. 62 ◽  
Author(s):  
Mathilde Janot ◽  
Marie-Laure Cortes-Dubly ◽  
Stéphane Rodriguez ◽  
Uyen Huynh-Do

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Jeremy W. Duncan ◽  
Matthew Bergeron ◽  
Jessica L. Bradshaw ◽  
Frank T. Spradley ◽  
Joey P. Granger

2017 ◽  
Vol 39 (1-4) ◽  
pp. 215-227 ◽  
Author(s):  
Annie R.A. McDougall ◽  
Vanny Wiradjaja ◽  
Aminath Azhan ◽  
Anqi Li ◽  
Nadia Hale ◽  
...  

Intrauterine growth restriction (IUGR) is a major cause of antenatal brain injury. We aimed to characterize cerebellar deficits following IUGR and to investigate the potential underlying cellular and molecular mechanisms. At embryonic day 18, pregnant rats underwent either sham surgery (controls; n = 23) or bilateral uterine vessel ligation to restrict blood flow to fetuses (IUGR; n = 20). Offspring were collected at postnatal day 2 (P2), P7, and P35. Body weights were reduced at P2, P7, and P35 in IUGR offspring (p < 0.05) compared with controls. At P7, the width of the external granule layer (EGL) was 30% greater in IUGR than control rats (p < 0.05); there was no difference in the width of the proliferative zone or in the density of Ki67-positive cells in the EGL. Bergmann glia were disorganized at P7 and P35 in IUGR pups, and by P35, there was a 10% decrease in Bergmann glial fiber density (p < 0.05) compared with controls. At P7, trophoblast antigen-2 (Trop2) mRNA and protein levels in the cerebellum were decreased by 88 and 40%, respectively, and astrotactin 1 mRNA levels were increased by 20% in the IUGR rats (p < 0.05) compared with controls; there was no difference in ASTN1 protein. The expressions of other factors known to regulate cerebellar development (astrotactin 2, brain-derived neurotrophic factor, erb-b2 receptor tyrosine kinase 4, neuregulin 1, sonic hedgehog and somatostatin) were not different between IUGR and control rats at P7 or P35. These data suggest that damage to the migratory scaffold (Bergmann glial fibers) and alterations in the genes that influence migration (Trop2 and Astn1) may underlie the deficits in postnatal cerebellar development following IUGR.


2021 ◽  
Vol 11 (1) ◽  
pp. 78
Author(s):  
Marcelo E. Rains ◽  
Colin B. Muncie ◽  
Yi Pang ◽  
Lir-Wan Fan ◽  
Lu-Tai Tien ◽  
...  

Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.


2002 ◽  
Vol 283 (1) ◽  
pp. E124-E131 ◽  
Author(s):  
Marie-Claude Battista ◽  
Luc L. Oligny ◽  
Jean St-Louis ◽  
Michèle Brochu

Epidemiological studies have produced evidence that unfavorable intrauterine environments during fetal life may lead to adverse outcomes in adulthood. We have previously shown that a low-sodium diet, given to pregnant rats over the last week of gestation, results in intrauterine growth restriction (IUGR). We hypothesize that pups born with IUGR are more susceptible to the development of hypertension in adulthood. IUGR fetuses and rats aged 1 wk were characterized for organ growth and renal morphogenesis. The adults (12 wk) were evaluated for weight, systolic blood pressure, activity of the renin-angiotensin-aldosterone system (RAAS), and renal function; hearts and kidneys underwent a histological examination. Brain and cardiac ventricle-to-body ratios were increased in IUGR fetuses compared with age-matched controls, whereas the kidney-to-body ratio was unchanged. Systolic blood pressure was elevated in both IUGR male and female adults. Plasma aldosterone levels were not correlated with increased plasma renin activity. Moreover, urinary sodium was decreased, whereas plasma urea was elevated in both males and females, and creatinine levels were augmented only in females, suggesting a glomerular filtration impairment in IUGR. In our model of IUGR induced by a low-sodium diet given to pregnant rats, high blood pressure, alteration of the RAAS, and renal dysfunction are observed in adult life. Differences observed between male and female adults suggest the importance of gender in outcomes in adulthood after IUGR.


Author(s):  
Jenny Voggel ◽  
Lubomir Lubomirov ◽  
Felix Lechner ◽  
Gregor Fink ◽  
Eva Nüsken ◽  
...  

Intrauterine growth restriction (IUGR) due to an adverse intrauterine environment predisposes to arterial hypertension and loss of kidney function. Here we investigated whether vascular dysregulation in renal interlobar arteries (RIA) may contribute to hypertensive glomerular damage after IUGR. In rats, IUGR was induced by bilateral uterine vessel ligation. Offspring of non-operated rats served as controls (C). From postnatal day (PND) 49, blood pressure was telemetrically recorded. On PND 70, we evaluated contractile function in RIA and mesenteric arteries (MA). Additionally, blood, urine and glomerular parameters and renal collagen deposition were analyzed. IUGR-RIA not only showed loss of stretch activation in 9/11 arteries and reduced stretch-induced myogenic tone, but also a shift of the concentration-response relation of acetylcholine-induced relaxation towards lower concentrations. However, IUGR-RIA also exhibited augmented contractions through phenylephrine (PE). Systemic mean arterial pressure [mean differences 4.8 (daytime) and 5.7 mmHg (night)], mean glomerular area (IUGR, 9754 ± 338; C, 8395 ± 227 µm2) and urinary protein/creatinine ratio (IUGR, 1.67 ± 0.13; C, 1.26 ± 0.10 g/g) were elevated after IUGR. We conclude that male IUGR rat offspring may have increased vulnerability towards hypertensive glomerular damage due to loss of myogenic tone and augmented endothelium-dependent relaxation in RIA.


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