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At least 19 recordsLinked to original sources
PubMed2026

Fetal hypoxia causes oocyte oxidative stress damage via the Sirt3/Sod2 pathway and can be alleviated by nicotinamide mononucleotide.

Environmental hypoxia exerts detrimental effects on the reproductive capabilities of both humans and animals. A fetal hypoxia model was established in which fetal mice were kept in a high-plateau hypoxic setting from embryonic day (E) 0 to 16.5. In our previous research, we found that fetal hypoxia exposure perturbs the methylation of imprinted genes in adult sperm and causes intergenerational placental impairments in male offspring. However, the specific impacts of fetal hypoxia on the female reproductive system, particularly regarding oocyte maturation, remain poorly understood. First, we found that fetal hypoxia mice exhibited a significant reduction in the average number of pups per litter. We conducted a comprehensive analysis of the transcriptome in oocytes from the hypoxic group and investigated the metabolic alterations within the follicular microenvironment. Fetal hypoxic stress contributed to cleavage and blastocyst rate reduction and induced early apoptosis and DNA damage triggered by mitochondrial dysfunction, oxidative stress aggravation and Sirt3/Sod2 downregulation. Additionally, administration of nicotinamide mononucleotide (NMN) has been shown to prevent oocytes from mitochondrial dysfunction and developmental impairment by increasing the expression of Sirt3/Sod2 and autophagy. The number of pups per litter in fetal hypoxia mice was reduced by 57.7% compared to the control group, while NMN intervention could restore it to 73.1% of the control group. These results indicate that fetal hypoxia exposure exerts multiple potential damages to adult female reproduction, while highlighting the clinical potential of NMN supplementation as a targeted intervention to alleviate such hypoxia-associated female reproductive impairment.

Animals↗
PubMed1978

[Diagnosis and outcome of cerebral distress in newborn infants who presented signs of fetal hypoxia. Prospective study].

The prospective study covered 60 full-term newborns, who presented exclusively signs of acute fetal distress. It had two major aims: --the analysis of the clinical and EEG symptomatologies, allowing the assessment of the cerebral damage in the neonatal period; --the evaluation as to whether the post-asphyxia cerebral damage may remain undiagnosed in the neonatal period, sequellae revealing it secondarily. Clinical and EEG supervision was undertaken during the first week; it was continued till 3 years of age in 45 of the 56 survivors. During the first week of life, 50 infants had at least once, an abnormal neurologic manifestation. The signs for a poor outcome are "unexpected" fetal distress, Apgar score below 2 at 1 min., seizures occurring or persisting after 48 hours, severe clinical and/or EEG changes occurring more than once. Prognosis is considered as favorable if EEG or clinical examination are consistently normal, or if EEG and clinical examination are normalized at 6 days of life.

Apgar Score↗
PubMed1976

[Acid-base equilibrium during acute fetal hypoxia. Experimental study].

The authors studied the effects of acute hypoxia of short duration in eight pregnant ewes that had been anaesthetised. They showed that during the experiment the E.E.G. as well as the pH and pCO and the maternal lactate levels were not changed and that therefore changes that can be found in the fetus are due solely to its own hypoxia and not due to transmission from the mother. In the fetus the trace flattens in about 30 minutes on an average. After this interval a moderate drop in pH occurs at the same time as an increase in lactacidemia and the relationship between lactate and pyruvate. The heart rate is changed in a variable manner: it accelerates if the basal rate is less than 180 beats a minute and slows if it is above 180. Blood pressure rises. Changes in the cardio-vascular system always precede those in the electroencephalograms.

Acid-Base Equilibrium↗
PubMed1975

Placenta to lamb fetus transfusion in utero during acute hypoxia.

Maternal and fetal hemodynamics, placental blood flow, fetal-placental blood volume, placental blood volume, and fetal blood volumes were measured in six chronic sheep prepartions to evaluate their changes during acute fetal hypoxia induced by maternal hypoxia. During fetal hypoxia, the maternal and fetal arterial blood pressure and heart rate were essentially unchanged. The placental blood flow (control equal to 325 ml.per kilogram per minute) was also unchanged during the hypoxia period. However, the placental blood volume decreased significantly from 65 to 60 and 51 ml. per kilogram at 15 and 30 minutes of hypoxia period, respectively. The fetal blood volume increased reciprocally and significantly from 86 to 109 and 102 ml. per kilogram at the same periods of hypoxia since the fetal-placental blood volumes were unchanged. These blood volume changes persisted for 30 to 60 minutes following the stoppage of hypoxia experiments. The placental vascular resistance measured in six experiments showed a significant increment during hypoxia, suggesting placental vasoconstriction as the responsible mechanism for the reduction of placental blood volume and reciprocal increase in fetal blood volume. The data suggest that significant placental transfusion to the lamb fetus may occur in utero during fetal hypoxia resulting in a higher fetal blood volume before birth.

Acute Disease↗
PubMed1978

Stimulation of fetal hemoglobin synthesis in baboons by hemolysis and hypoxia.

Fetal hemoglobin (Hb F) levels in the peripheral blood of baboons (Papio cynocephalus) increased from an average value of 0.78% to 18.1% during the recovery phase from phenylhydrazine-induced hemolytic anemia. A similar increase was observed in animals exposed to hypobaric hypoxia. Large individual variations in the maximal Hb F levels were observed which could not be correlated with the ages of the animals. Reinduction of hemolysis in two fully recovered animals resulted in Hb F levels that were of similar magnitude as in the preceding episode, suggesting the possibility of genetically determined individual variations in the rate of Hb F synthesis under the same conditions of erythropoietic stimulation. Reticulocytes from the animals subjected to hemolysis of hypobaric hypoxia synthesized similar absolute quantities of Hb F in vitro. The results of the present studies indicate that the physiological switch from the synthesis of Hb F to that of Hb A during ontogeny can be reversed in adult nonhuman primates by conditions of erythropoietic stress known to be associated with high erythropoietin levels. These findings open the possibility that Hb F synthesis in adult humans may be therapeutically modulated in individuals who might benefit from increased levels of Hb F, such as patients with sickle cell anemia.

Anemia, Hemolytic↗
PubMed1979

Human fetal oxygenation following paracervical block.

To test the hypothesis that fetal heart rate (FHR) changes following paracervical block may be secondary to fetal hypoxia, human fetal oxygenation was measured continuously using a transcutaneous electrode. Following the block, each fetus demonstrated a decline in oxygen tension (tcPO2) at 5 minutes, which reached its lowest value at a mean of 11.5 minutes and remained at this level for an average of 3 minutes. Following the block, FHR variability increased at 5.2 minutes. reaching its maximal level by a mean of 7.5 minutes. By 11 minutes, a decrease in FHR variability was noted, which lasted for approximately 17 minutes. Decreased variability was not uniformly associated with low tcPO2. On some occasions, fetal tcPO2 declined even in the absence of increased uterine activity, which was noted at times following the block. The severity of the tcPO2 decline appears related to the analgesic effectiveness of the block.

Anesthesia, Local↗
PubMed1976

Endocrine and metabolic changes associated with periods of spontaneous hypoxia in fetal sheep.

Periods of spontaneously occurring hypoxia have been observed in fetal sheep. These were associated with increases in the fetal plasma concentration of glucose, lactate, free fatty acids, ACTH and corticosteroids (for a fetus close to term). These changes are similar to those observed during experimentally induced hypoxia. Hypoxia may be a mechanism by which plasma metabolites and ACTH are increased in fetal sheep under physiological conditions, particularly during labour.

Adrenal Cortex Hormones↗
PubMed1979

Redistribution of cardiac output and oxygen delivery in the hypoxemic fetal lamb.

In hypoxia, fetal cardiac output and the product arterial O2 content x blood flow to the fetal heart and central nervous system (CNS) tend to remain constant. As a consequence the percentage of cardiac output directed to the heart and CNS increases hyperbolically in inverse relation to the oxygen content of the fetal ascending aorta, [O2]as. The fetal lamb maintains [O2]as approximately 0.45 mM (0.45 +/- 0.02 SEM) higher than the O2 content in the abdominal aorta, [O2]ab, over a wide range of oxygenation. When [O2]as decreases below the 2 mM level, the [O2]as--[O2]ab difference (delta O2) decreases also. A mathematical model of the fetal circulation shows that delta O2 is a function of the ratio oxygen consumption of fetal upper body/abdominal aorta blood flow (VU/FA). The behavior of delta O2 in hypoxia can be explained by assuming that the VU/FA ratio is maintained in moderate hypoxia and decreases in sever hypoxia.

Animals↗