PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MATERNAL-FETAL EXCHANGE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1977

Withdrawal syndrome upon cessation of chronic clonidine treatment in rats.

Clinical reports indicate that cessation of treatment with the antihypertensive agent clonidine is associated with a withdrawal syndrome which may include a hypertensive overshoot of critical proportions. We have attempted to produce an animal model of this syndrome in rats. Rats were treated with clonidine in the drinking water (5 microgram/ml; total dose 300-500 microgram/kg/day) which produced a significant (approx. 20%) decrease in heart rate and blood pressure. Within 24 h of cessation of treatment a significantly greater (approximately 100 beats/min) heart rate was seen in treated animals than in control animals when measurements were made in conscious animals. No hypertensive overshoot was observed. Cessation of treatment was associated with an increase in sympatho-adrenal tone as shown by a trans-synaptic induction of adrenal tyrosine hydroxylase activity. Adrenal denervation prevented the rise in adrenal tyrosine hydroxylase seen after cessation of treatment. Administration of clonidine to pregnant rats (10th day until term) did not alter the development of adrenal tyrosine hydroxylase in the offspring. The data indicate that a withdrawal syndrome is produced upon cessation of chronic clonidine treatment.

Adrenal Glands↗
PubMed1976

The meaning of the Leydig cell in relation to the etiology of cryptorchidism: An experimental electron-microscopic study.

In our electron-microscopic studies of testicular biopsies, both normal and cryptorchid, we found a simple atrophy of the Leydig cell in the cryptorchid testis. Based on experiments by Raynaud1,2 and Jean3 on pregnant mice, we tried to find the reason for changes in the Leydig cell relating to the etiology of cryptorchidism. We found on electron microscopic study of testes in the offspring of pregnant mice treated with estrogen the same atrophy of the Leydig cell as we see in human cryptorchidism. These changes are not evident when estrogen and HCG are given together. We can conclude from this experiment that lack of gonadotropin stimulation leads to the atrophy of Leydig cells. This atrophy then produces a lack of androgen which could be responsible for cryptorchidism.

Androgens↗
PubMed1978

Hemoglobin-ligand interaction in fetal and maternal sheep blood.

Hemoglobin-ligand interaction was studied in maternal and fetal sheep blood as a function of oxygen saturation. pH was changed by varying CO2 concentration (CO2 Bohr effect) or by addition of NaOH or HCl at constant PCO2 (fixed acid Bohr effect). For maternal blood, CO2 Bohr factor was -0.41 at 50% oxygen saturation, increasing in magnitude at lower saturation and decreasing in magnitude at higher saturation. For fetal blood, CO2 Bohr factor was -0.45 at 50% oxygen saturation, unchanging at lower saturation and decreasing in magnitude at higher saturation. Fixed acid Bohr factor was relatively saturation independent with a value of -0.36 for fetal blood and -0.27 for maternal blood. The pH-independent effect of molecular CO2 on oxygen affinity was markedly saturation dependent being greatest at low oxygen saturation. The CO2 effect was greater in maternal blood than fetal blood. However, the magnitude of the saturation dependency of Bohr factor is not great enough to have major physiological significance in oxygen transfer across the sheep placenta.

Animals↗
PubMed1976

On the influence of prostaglandin F2alpha-induced labor at term on the metabolism and coagulation of mother and fetus.

11 pregnancies at term were terminated by dilatation of the uterine cervix, low amniotomy, and by intravenous administration of PGF2alpha. The average infusion time was 3 hours 55 minutes, and the average total dose of PGF2alpha amounted to 2.0 mg. Parameters of acid-base changes, carbohydrate and energic state changes, gas metabolism, and changes in coagulation and fibrinolysis in mother and in fetus were analyzed during labor and after birth. Labor activity and fetal cardiac action were monitored cardiotocographically. Checked against 50 uncomplicated spontaneous deliveries, we found no disadvantageous changes in the parameters investigated.

Acid-Base Equilibrium↗
PubMed1977

Teratological study of etoperidone in the rat and rabbit.

Etoperidone was administered to pregnant rats and rabbits during the period of organogenesis. The oral doses were 100 and 300 mg/kg in the rat and 5, 25 and 50 mg/kg in the rabbit. In the rat the dose of 300 mg/kg produced toxic effects on the mother, consisting mainly of behavioural changes and death in some cases; a slight increase in embryofetal mortality was also observed. The dose of 100 mg/kg still produced behavioural changes in the mother, but had no effect on the product of conception. Chlorcyclizine, on the other hand, used as a reference drug in the rat produced fetal malformations at a dose devoid of any toxic activity on the maternal organism. The doses studied in the rabbit were shown to be pharmacologically active in the mothers, producing sedation. No effect, however, was observed on embryofetal development.

Animals↗
PubMed1976

Absorption, utilization, and safety of aspartic acid.

The dicarboxylic amino acids, asparate and glutamate, occupy unique positions in intermediary metabolism, particularly in the mitochondria, where they play important roles in nitrogen and energy metabolism. Administration of large quantities of glutamate and asparate to the newborn mouse produces a variety of neurotoxic effects, the most marked of which is neuronal necrosis. Neurotoxic effects of glutamate and aspartate in animal species other than the rodent are highly controversial. In the most critical animal species, the infant subhuman primate, at least four research groups have failed to duplicate the original report of glutamate-induced neuronal necrosis. Marked elevations in plasma glutamate or aspartate must occur for development of neuronal necrosis. In the highly sensitive neonatal mouse, plasma glutamate plus plasma aspartate levels must reach 60-80 mumol/dl to produce even minimal neuronal necrosis. In the healthy neonatal primate, loads producing plasma glutamate levels ranging from 50 to 1,600 mumol/dl failed to produce neuronal necrosis in our studies. Thus, it is clear that (1) marked elevations in plasma glutamate and aspartate must occur for neuronal necrosis, and (2) threshold levels required to produce neuronal necrosis vary greatly with species. The available data indicate little danger to the healthy primate and humans from ingestion of the dicarboxylic amino acids under anything resembling a reasonable intake. However, there is no doubt that these amino acids are toxic to the neonatal mouse at high dose levels.

Animals↗
PubMed1978

Placental transfer of lidocaine: effects of fetal acidosis.

To investigate whether fetal acidosis increases the placental transfer of lidocaine, resulting in higher fetal blood levels of the drug, lidocaine was infused intravenously into ten pregnant ewes to maintain plasma levels of 2-4 microgram/ml. After maternal-fetal equilibrium was reached, the fetus was made acidotic by infusing lactic acid intravenously. Fetal blood pH decreased from 7.35 to 7.10. With fetal acidemia, fetal blood lidocaine levels increased significantly from 1.60 +/- 0.11 microgram/ml to 2.72 +/- 0.26 microgram/ml. The fetal-maternal lidocaine ratio increased from 0.76 to 1.21. Correction of the acidosis by bicarbonate infusion returned the fetal-maternal ratios to control values. It is concluded that acidosis in the fetus may result in trapping of ionized lidocaine in the fetal circulation and increase the transfer of lidocaine across the placenta.

Acidosis↗