GOT<i>PURE</i>BLOOD IN FETAL RATS?

Mao, Caiping; Guan, Jun; Yuan, Xin; Miao, Y.; Zhu, Hong; Chen, L; Lv, Jian; Xu, Fulin; Liu, Y; Hui, Pengpeng; Zhu, Yi; Xu, Zhice

doi:10.1080/08880010701451467

Cited by 6 publications

(7 citation statements)

References 3 publications

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“…Fetal growth restriction in human (Regnault et al, 2007), and in large and small animals (Bauer et al, 2007), can be caused by multiple mechanisms, including in utero hypoxia (Viswanathan et al, 2007). It has been shown that maternal nicotine administration decreases fetal blood PO 2 in animals including rats (Socol et al, 1982;Mao et al, 2007). Notably, fetal brain weight was also significantly decreased by nicotine treatment in the present study.…”

Section: Discussionsupporting

confidence: 67%

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

Mao

Zhu

et al. 2008

NeuroToxicology

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Previous studies have suggested that prenatal exposure to nicotine is associated with abnormal development in fetuses, including fetal brain damage. The present study determined the effect of maternal administration of nicotine during different gestational periods on brain nicotine receptor subunits in fetal rats. Subcutaneous injections of nicotine in maternal rats from the early and middle gestation decreased fetal blood PO 2 , increased fetal blood PCO 2 and hemoglobin, and decreased fetal brain weight. The nicotinic acetylcholine receptor (nAChRs) mRNA abundance in the fetal brain was significantly changed by prenatal treatment with nicotine during pregnancy. Fetal α2, α4, α7, and β2 units were significantly increased in the brain by prenatal exposure to nicotine in rat fetuses. However, the expression of mRNA of fetal brain α3, α5, β3, and β4 units were not changed. The results showed that prenatal nicotine can change the development of both α and β subunits of nAChRs in the fetal brain at gene level in association with restriction of fetal brain growth and in utero hypoxia.

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Section: Discussionsupporting

confidence: 67%

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

Mao

Zhu

et al. 2008

NeuroToxicology

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“…This makes analysis of blood values complicated and difficult. In the present study, we developed a method to collect fetal blood samples directly from the fetal heart in fetal rats for measurement of blood pO 2 , pCO 2 , O 2 saturation, pH, and lactic acid (Mao et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The effect of prenatal nicotine on mRNA of central cholinergic markers and hematological parameters in rat fetuses

Mao

Yuan²,

Zhang³

et al. 2008

Intl J of Devlp Neuroscience

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A number of studies have demonstrated the influence of nicotine on fetal development. This study determined the expression of choline acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT), and high-affinity choline transporter (CHT1) in the forebrain and hindbrain following chronic prenatal nicotine exposure in the rat fetus (maternal rats were subcutaneously injected with nicotine at different gestation periods). We also measured the effect of chronic nicotine exposure on fetal blood pO 2 , pCO 2 , pH, Na + and K + concentrations, as well as lactic acid levels. Maternal nicotine exposure during pregnancy was associated with a decrease in fetal pO 2 coupled with a significant increase in pCO 2 and lactic acid as well as restricted fetal growth. Additionally, maternal nicotine administration also reduced ChAT, VAChT, and CHT1 mRNA levels in the fetal brain. Nicotineinduced fetal hypoxic responses and reduced cholinergic marker expression in the brain were more severe when nicotine was started in early gestation. Our results provide new information about the effects of repeated exposure to nicotine in utero on the expression of central ChAT, VAChT, and CHT1 in the rat fetus. These results indicate that repeated hypoxic episodes or/and a direct effect of nicotine on the central cholinergic system during pregnancy may contribute to brain developmental problems in fetal origin.

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“…Several important nuclei located around the ventricular area, including the paraventricular nuclei, subfornical organ, median preoptic nuclei, and supraoptic nuclei, play an important role in water and salt intake in response to i.c.v. Ang II (Fitzsimons, 1998; Davisson et al, 2000; Mao et al, 2007a, b). Those areas around the ventricular system are also rich of Ang II receptors (Fitzsimons, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Maternal, fetal, and adult offspring blood samples were collected into ice-cold plastic tubes as reported (Mao et al, 2007a, b). Briefly, fetal blood samples (7–8 fetuses from the same dam as n =1, and n =6–8, each group) were collected directly from the heart using intracardiac puncture, and blood was pooled together in the same litter.…”

Section: Methodsmentioning

confidence: 99%

Prenatal water deprivation alters brain angiotensin system and dipsogenic changes in the offspring

et al. 2011

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Objective Central renin–angiotensin system (RAS) plays an important role in regulating body fluid balance. The present study determined the effect of maternal dehydration on brain expression levels of angiotensinogen, angiotensin II receptor subtypes, and dipsogenic responses in offspring. Methods Pregnant rats were deprived of water during late gestation. Expressions of brain angiotensinogen, angiotensin II receptors, and dipsogenic responses were determined. Results Maternal water deprivation significantly decreased fetal body and brain weight, and body and tail length. Fetal plasma sodium, osmolality, and hematocrit were increased. Both AT1R and AT2R protein abundance was significantly increased in the fetal brain, associating with increased mRNA levels of AT1aR and AT2R. Additionally, angiotensinogen mRNA was increased. In adult offspring, prenatal dehydration resulted in significant increases in AT1R protein and AT1aR mRNA, as well as angiotensinogen mRNA in the forebrain in both males and females. In contrast, AT2R mRNA and protein were increased only in males. Prenatal dehydration resulted in a significant increase in intracerebroventricular angiotensin II-induced water intake in male, but not female, offspring. Conclusion The results provided new information that antenatal water deprivation induces a reprogramming of brain RAS and Ang II receptor expression patterns and alters the central Ang II-mediated dipsogenic response in offspring in a sex-dependent manner.

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GOTPUREBLOOD IN FETAL RATS?

Cited by 6 publications

References 3 publications

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

The effect of prenatal nicotine on mRNA of central cholinergic markers and hematological parameters in rat fetuses

Prenatal water deprivation alters brain angiotensin system and dipsogenic changes in the offspring

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