Biomedical subjects

R A Chez

Publications and source records attributed to R A Chez.

At least 109 records · Page 6Linked to original sources

PubMed1976

Uteroplacental blood flow during hyperthermia with and without respiratory alkalosis.

The effect of induced maternal hyperthermia (1.5 degrees C rise over 60 min) on the uterine and umbilical circulations was examined in two groups of chronically instrumented pregnant sheep. Hyperventilation occurred in both groups. In the group in which the resultant respiratory alkalosis was untreated (N = 5), uterine blood flow decreased to 53 +/- 3% (mean +/- SE; P less than 0.01) of control at maximal maternal temperature. Umbilical blood flow also decreased 30 +/- 6% (P less than 0.01) below control levels. In the other group, normocapnia was maintained (N = 4). Uterine blood flow decreased in this group to 75% +/- 2% (P less than 0.01) of control levels, but umbilical blood flow did not significantly change. There was no significant change in maternal or fetal mean arterial pressure during hyperthermia in either group. Thus, maternal hyperthermia per se results in a significant decrease in uterine blood flow primarily through an effect on uterine vascular resistance, but without a concomitant change in umbilical blood flow.

Alkalosis, Respiratory↗

PubMed1976

Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep.

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2-16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100-200 mg/kg. Mean fetal arterial Pco2 increased from 49.5 to 63.4 mmHg but no significant changes in umbilical blood flow occurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. No dignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despite an increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistance did not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor in normal physiological regulation of the uteroplacental circulation in this species.

Acetazolamide↗

PubMed1976

Lung lecithin biosynthesis in the nonhuman primate fetus: determination of the primary pathway in vivo.

The two pathways for de novo lecithin (phosphatidylcholine) biosynthesis, choline incorporation (1) and phosphatidylethanolamine methylation (II), were examined simultaneously in lung and other tissues of Rhesus monkey fetuses. Cannulation of interplacental fetal vessels permitted studies on the intrauterine fetus without disruption of fetal-placental-maternal-amniotic fluid anatomic integrity. In contrast to observations with indirect techniques in the same species, direct measurement of the incorporation of isotopic precursors (3H-choline and 14C-ethanolamine) into lecithin indicated that pathway I predominates by 100-fold over PE methylation in pulmonary lecithin synthesis. Fetal liver, brain, and kidney also showed 10--70-gold greater choline incorporation that methylation activity. Measurement of lung phosphatidylcholine production via the two pathways in acidemic fetuses (umbilical venous pH less than 7.20) demonstrated marked inhibition of pathway I, but not II. It is concluded that the choline pathway is the major mechanism of lung lecithin synthesis in fetal primates and that this pathway is pH sensitive in vivo.

Acid-Base Equilibrium↗

PubMed1976

Glycogen regulation in isolated perfused near term monkey liver.

Glycogen metabolism was studied in the isolated perfused liver of the monkey conceptus at 90% of gestation using an in situ recirculating perfusion system. Net uptake of glucose and galactose and the activities of the enzymes, glycogen synthetase and phosphorylase, were studied in response to varied perfusate composition. Synthetase activity was expressed as %I. the percentage of total synthetase activity in the active form. Perfusate glucose concentrations as high as 700 mg/100 ml did not lead to net glucose uptake of to an increase in the baseline %I synthetase (4 +/- 1, mean +/- SEM). In the presence of 300 mg/100 ml glucose, insulin at 10(-7) M in creased %I to 8 +/- 2, and galactose greater than 75 mg/100 ml increased %I to 8 +/- 1. The combination of galactose, glucose, and insulin increased %I to 40 +/- 5. With this latter combination, synthetase activity was proportional to perfusate glucose concentration above 100 mg/100 ml. Phosphorylase activity was diminished by either galactose or insulin, and phosphorylase activity was lowest in the group receiving galactose, glucose, and insulin. Galactose was taken up by all livers, but net glucose uptake was not observed under any condition; net hexose uptake was observed in perfusions with galactose. Glycogen levels did not vary significantly with varied perfusate composition during the 30-min perfusion periods.

Animals↗

PubMed1976

Hypothalamic-pituitary control of perinatal prolactin secretion in Macaca mulatta.

Sequential changes in maternal and fetal plasma and amniotic fluid concentrations of prolactin (PRL) and growth hormone (GH) were examined after these intravascular administration of thyrotropin releasing hormone (TRH) or L-dopa alone or combined directly to the near-term Rhesus fetus. The neonatal plasma responses to these same stimuli were also examined. Fetal and neonatal plasma PRL levels increased immediately after TRH injection and remained elevated from baseline levels (102-800%) throughout the 45 min sampling period. Maternal plasma PRL levels also increased markedly. Although amniotic fluid concentrations were more variable, the trend was an increase. After L-dopa injection, fetal and neonatal plasma PRL values declined 26-62% from baseline levels. Maternal plasma PRL concentrations also declined 30-50%, but amniotic fluid PRL concentrations progressively increased. When L-dopa and TRH were administered together, fetal plasma PRL levels declined 14-40% from initial levels, but maternal plasma PRL levels did not change in a consistent manner, and amniotic fluid PRL levels remained stable. There was no change from baseline fetal or neonatal plasma GH concentrations in these experiments. The plasma PRL responses of the primate conceptus to these stimuli are consistent with those found in the adult; the unresponsiveness of plasma GH is not. The direction and magnitude of changes in both maternal plasma and amniotic fluid PRL concentrations provide indirect evidence of placental transfer of TRH and L-dopa in some experiments, and require a biophysical explanation not apparent in others.

Amniotic Fluid↗

PubMed1976

Nonhuman primate models of toxemia of pregnancy.

Hypertension in the nonpregnant and pregnant nonhuman primate is not found frequently by research investigators. Its incidence is probably infrequent. No well-defined clinical syndrome analogous to toxemia of human pregnancy has been described. The experimental induction of the disease in pregnant nonhuman primates has been difficult. Although there would be an important role for such an animal model, its discovery does not appear imminent.

Animals↗

PubMed1976

Fetal lung lecithin metabolism in the glucose-intolerant Rhesus monkey pregnancy.

Fetal lung lecithin metabolism was examined in rhesus monkey gestations complicated by glucose intolerance secondary to maternal streptozotocin (STZ) administration. Fetuses of STZ-treated mothers were delivered at 85% to 89% of term and were compared to two control groups of fetuses from normal pregnancies--one group age-matched to the STZ pregnancies, and the other composed of fetuses delivered in the final 10% of gestation. In the glucose-intolerant pregnancies, two measures of fetal lung lecithin biosynthesis--the amniotic fluid lecithin-to-sphingomyelin (L/S) ratio and the rate of 14C-choline incorporation into lecithin in fetal lung slices--were significantly greater than in age-matched normal gestations and were similar to results in late-gestation controls. However, lung lecithin concentrations in the glucose-intolerant group were comparable to the age-matched controls, and both were significantly less than in the late-gestation controls. Since the gestational age, mode of delivery, and fetal acid-base status were the same in the age-matched groups, we conclude that these changes in fetal lung lecithin metabolism are due to the effects of maternal glucose intolerance.

Amniotic Fluid↗

PubMed1976

Two operative technics applied in perinatal research in the rhesus monkey.

Methods for percutaneous transabdominal amniocentesis and umbilical artery cannulation as modified and applied to the perinatal study of the rhesus monkey were described. These technics proved to be reliable, reproducible, and safe when used with care and attention to sterile technic.

Amniocentesis↗

PubMed1976

A system for inducing hyperthermia in sheep.

A system that produces hyperthermia in pregnant sheep in a consistent and reproducible manner was designed. The experimental approach was through control of ambient temperature and relative humidity in a closed chamber; the sheep was unable to lose its metabolic heat in an environment of 42 degrees C and 75% relative humidity. This system resulted in a steady and progressive temperature rise of 2.5 degrees C in the maternal abdominal aorta in 120 +/- 17 min.

Animals↗

PubMed1975

Maternal-fetal plasma glucose relationships in late monkey pregnancy.

Maternal hyperglycemia was induced in six late gestation monkey pregnancies with intravenous glucose injection plus infusion. The maximum measured plasma glucose levels of the mother varied from 380 to 1,020 Gm. per cent. A significant linear relationship evolved between maternal and fetal plasma glucose peak concentrations. A saturation limit to placental transfer of glucose across the placenta is not apparent from these data.

Animals↗

PubMed1975

Sonar biparietal diameter growth standards in the rhesus monkey.

Serial sonar fetal cephalometry was performed on 67 pregnant monkeys (Macaca ulatta) with known breeding dates. A normal biparietal diameter (BPD) growth curve was constructed along four percentile divisions; namely, the 10th to the 24th, 25th to the 49th, 50th to the 74th, and the 75th to the 90th. It is shown that under normal conditions fetuses initially positioned in any one of these divisions will continue to grow within the confines of that same percentile range. This biologic phenomenon has not been previously reported. It is significant because it leads to a more precise separation of normal vs. suboptimal intrauterine growth.

Animals↗

PubMed1975

Plasma renin activity during ovine pregnancy.

Chronic intravascular catheterization in maternal, fetal, and neonatal sheep was utilized to assess basal plasma renin activity (PRA) and changes in PRA in response to furosemide. Maternal PRA increased from base-line levels during the last trimester of pregnancy and remained elevated for 12 wk postpartum. Fetal basal levels of PRA were variable but usually greater than maternal levels. Intravenous administration of furosemide to pregnant ewes resulted in a prompt and significant increase in maternal PRA with inconsistent changes in fetal PRA. Fetal and neonatal animals with low basal levels showed a significant increase in PRA; maternal PRA did not change. Animals with higher basal levels did not respond to the stimulus, perhaps reflecting a maximum renin secretory rate. These data are consistent with the conclusions that fetal renin originated predominantly from the fetal kidney, that fetal PRA receives no significant contribution from the maternal circulation, and that renin does not cross the ovine placenta.

Animals↗

PubMed1975

Perinatal primate parathyroid hormone metabolism.

Near-term fetal and neonatal parathyroid gland function has been studied in the Rhesus monkey. Fetal serum ionized calcium (Ca++) levels are significantly greater than simultaneously obtained maternal levels. Fetal serum parathyroid hormone (PTH) was undetectable both in the basal state and in association with EDTA-induced fetal hypocalcemia. Induced maternal hypocalcemia was associated with increased maternal serum PTH levels and no change in fetal basal serum Ca++ or PTH levels. Only a minimal decrease in simian neonatal serum Ca++ occurred over the first 48 h of life. Normal adult levels of serum PTH were present as early as 6 h of neonatal life. Induced hypocalcemia at 12 h of age resulted in a significant increase in serum PTH levels.

Animals↗

PubMed1975

Glucose regulation by isolated near term fetal monkey liver.

Near term fetal monkey livers were perfused with a closed recirculating system and a defined perfusion medium. Livers from normal fetal animals were able to release glucose rapidly into the perfusate when they were exposed to glucagon, cyclic AMP, or an aglycemic perfusate, but they did not remove glucose rapidly from the perfusate, synthesize glycogen, or activate liver glycogen synthetase in response to hyperglycemia (Figs. 1,2, and 3; Table 1). Insulin decreased glucose mobilization in response to aglycemia, but did not stimulate glucose uptake during hyperglycemia; insulin activated glycogen synthetase (Table 1; Figs. 1 and 3). Livers from fetuses of streptozotocin-treated mothers and livers from 2-week-old neonates released more glucose into the perfusate in response to aglycemia then did livers from normal fetal monkeys (Fig. 4). These observations support the possibility that neonatal monkey liver is capable of rapidly mobilizing glucose during periods of hypoglycemia but is unable to take up glucose and store glycogen rapidly during periods of hyperglycemia.

Adenosine Monophosphate↗

PubMed1975