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S S Daniel

Publications and source records attributed to S S Daniel.

11 recordsLinked to original sources
PubMed1992

Long-term acid-base measurements in the fetal and maternal baboon.

OBJECTIVE: The purpose of the study was to examine the relationship between maternal and fetal acid-base indexes in the baboon. STUDY DESIGN: Eight animals maintained in a tether system were studied during the third trimester. Results were analyzed using analysis of variance. RESULTS: After recovery from surgery, pH in carotid artery blood of the fetus was 7.40 +/- 0.027 (mean +/- SD), PO2, 27.5 +/- 3.45 mm Hg; PCO2, 34.0 +/- 2.37 mm Hg; base deficit, 3.0 +/- 2.15 mEq/L; Hot, 33.4% +/- 2.69% and HbO2, 61.3% +/- 8.65%. The corresponding values in the mother were 7.48 +/- 0.035, 100.7 +/- 9.44 mm Hg, 26.4 +/- 2.95 mm Hg, 3.6 +/- 1.71 mEq/L, 32.6% +/- 4.0% and 97.9% +/- 1.28%, respectively. All indexes remained essentially the same until the onset of active labor, at which time the fetus became slightly acidotic and hypoxemic (pH less than 7.35, HbO2 less than 50%). CONCLUSION: The baboon fetus has slightly higher pH2 and lower PaCO2 than the human fetus and PaO2, base deficit, and maternal-fetal gradients across the placenta in these two primate species are comparable.

Acid-Base Equilibrium↗
PubMed1991

Effects of Ro 15-4513 on ethanol discrimination in C57BL/6 mice.

Ro 15-4513, a partial benzodiazepine receptor inverse agonist, counteracts many of the effects of ethanol, however, its effects on ethanol discrimination in operant paradigms remains unclear. The present study examined the effects of Ro 15-4513 on ethanol discrimination by female C57BL/6 mice in a food-reinforced behavior-operant paradigm. Under the time and dosing conditions used in previous reports, Ro 15-4513 did not alter ethanol discrimination whether given prior to or after ethanol exposure. The drug did, however, attenuate ethanol discrimination for brief periods (less than 8 min) when injected after ethanol and at doses and postinjection times which also disrupted responding. The present study confirmed that Ro 15-4513 attenuated ethanol discrimination, but not to the extent as previously reported. The results indicate that postinjection time is a very critical factor in whether Ro 15-4513 attenuates ethanol discrimination.

Animals↗
PubMed1979

Arginine vasopressin during gestation and parturition in sheep fetus.

The possible correlation between plasma arginine vasopressin (AVP) concentration and the processes leading to parturition was assessed in 11 chronically catheterized pregnant ewes. Samples of blood withdrawn intermittently during a 20-day period preceding labor and during parturition were analyzed for AVP by a specific radioimmunoassay, as well as for pH, PaCO2 and PaO2. Fetal AVP was 1.74 +/- 1.55 pg/ml and maternal AVP 1.47 +/- 0.74 pg/ml (mean +/- SD). No preparturient rise in fetal vasopressin was noted, but levels increased progressively during labor to reach peak levels in cord blood (range 7.5--8,000 pg/ml). There was no consistent rise in maternal vasopressin during the same interval. A relationship between prolonged antepartum intrauterine asphyxia and increases in fetal vasopressin was noted. It is concluded that the markedly elevated levels of vasopressin observed in cord blood are the result of intrapartum 'stress', but are not related to the initiation of parturition.

Animals↗
PubMed1978

Renal response of fetal lamb to complete occlusion of umbilical cord.

The renal response of the fetal lamb to repeated complete occlusion of the umbilical cord was studied in nine chronically instrumented animals. Five episodes of occlusion of the umbilical cord, each lasting for two minutes, produced a twofold rise in fetal urine osmolality and sodium, chloride, and potassium concentrations. Output of urine and glomerular filtration rate remained essentially unchanged while free water clearance decreased from a control of +0.10 to -0.02 ml. per kilogram per minute at the end of the fifth episode. Electrolyte concentrations in urine remained elevated for at least two hours following the occlusions. In addition to changes in urine composition, there was a 50- to 200-fold increase in the fetal plasma concentration of vasopressin. These studies indicate that complete interruption of the umbilical circulation, even though of short duration, produces disturbances in fetal renal function that can lead to loss of electrolytes in the urine. They provide an explanation for the low sodium levels reported in asphyxiated newborn infants in renal failure.

Acid-Base Equilibrium↗
PubMed1977

Effects of terbutaline on the pregnant baboon and fetus.

The effects of terbutaline on the mother and fetus were evaluated in 8 near-term pregnant baboons. Significant suppression of postoperative spontaneous and oxytocin-augmented uterine activity was achieved with infusion rates of 0.36 and 0.56 microgram/kg/min, respectively. Maternal and fetal blood pressure and acid-base states as well as fetal heart rate were unaffected by the administration of terbutaline to the mother, but a mild maternal tachycardia was observed. Both maternal and fetal blood glucose increased during terbutaline infusion. Direct administration of terbutaline to the fetus did not alter the fetal cardiovascular or acid-base state. It is concluded that in the baboon, terbutaline is an effective tocolytic agent with minimal untoward effects on either mother or fetus.

Acid-Base Equilibrium↗
PubMed1976

Umbilical vein occlusion and transient acceleration of the fetal heart rate. Experimental observations in subhuman primates.

Transient acceleration of the fetal heart rate is commonly seen in the cardiotachometer tracing of the human fetus during labor. A likely cause appeared to be partial occlusion of the umbilical cord. On the basis of this hypothesis, fetal cardiovascular responses to partial occlusion of the umbilical cord or isolated intra-abdominal portion of umbilical vein were studied in near-term pregnant baboons and rhesus monkeys prior to and following sympathetic blockade with dibenzyline and propranolol. The responses were of two types. In the well-oxygenated fetus, partial occlusion resulted in transient acceleration of heart rate and a decrease in pulse pressure. This response was abolished with dibenzyline or propranolol. In the hypoxic fetus, partial occlusion resulted in either bradycardia and hypotension or hypotension with no alteration in heart rate. Thus, transient acceleration of the fetal heart rate can be explained on the basis of a sympathetic response to diminished venous return. It would appear to be an early sign of a potential cord complication. This response will not be seen if the fetus becomes asphyxiated and hypoxic.

Animals↗
PubMed1976

The hemodynamic effects of intrauterine hypoxia: an experimental model in newborn lambs.

An experimental animal model of intrauterine hypoxia and respiratory distress in newborn lambs was produced by inducing maternal hypotension. Serial hemodynamic data indicated that the oxygenation defect in the lambs was due to right-to-left shunting of blood through fetal channels rather than within the lungs. Shunting was mainly across the foramen ovale, but, in severely distressed animals, significant right-to-left shunt also occurred through the ductus arteriosus. Left-to-right shunts across the ductus arteriosus were found in lambs with milder respiratory distress. The implications of perinatal hypoxia as it affects the pulmonary vascular bed in human neonates with the respiratory distress syndrome (hyaline membrane disease) and persistence of the fetal circulation are discussed. It is speculated that the early pulmonary vascular esponses in the two diseases may be identical.

Animals↗
PubMed1975

The effect of increased maternal PaO2 upon the fetus during labor.

The effect of increased maternal PaO2 upon the fetus during labor was studied in 36 subhuman primates. The animals were divided into two groups, one in which the fetus was not asphyxiated and showed no evidence of fetal distress (Group I) and another in which the fetus was acidotic, hypoxic, and exhibited the pattern of late deceleration of the heart rate (Group II). One hundred per cent oxygen was administered to the mothers for a period of 30 minutes. Elevation of maternal PaO2 to 430 mm. Hg increased fetal oxygen levels in Group I. and in most instances in Group II, without significant changes in the acid-base state. In Group II, maternal hyperoxemia also abolished or reduced the frequency of late deceleration of the fetal heart in most animals but had little or no effect on fetal blood pressure. Termination of high-concentration oxygen to the mother resulted in a fall in maternal and fetal oxygen levels to their original values and the reappearance of late fetal heart decelerations. Thus, administration of high-concentration oxygen to the mother for the treatment of fetal distress may be of some benefit. The problems of fetal acidosis and hypotension are not cured, however, and may still progress if there is placental insufficiency or cord compression. Therefore, this treatment should be regarded as a temporary supportive measure only.

Acid-Base Equilibrium↗
PubMed1975

Renal response of the lamb fetus to partial occlusion of the umbilical cord.

The role of the fetal kidney during impairment of placental exchange was studied in eight fetal lambs, intact in utero; a standard asphyxial insult for a period of 1 hour was produced by occluding the umbilical cord sufficiently to lower the fetal heart rate by 35 +/- 5 beats/min and the pH by 0.15 units. This asphyxial stress caused a fall in urine output from a control of 0.17 to 0.03 ml/kg/min and of glomerular filtration rate from 1.2 to 0.3 ml/min; release of the occlusion was followed by mild diuresis. The fall in urine output was accompanied by a rise in total primary solutes including concentrations of electrolytes; this rise continued for 1 to 2 hours following the release of the occlusion. Because of the low urinary output during the period of occlusion, there was a fall in excretion of electrolyte; an increase in net acid excretion occurred only after the release of the cord. These experiments show that, although the fetal kidney is capable of contributing to elimination of acid following compression of the cord, there may be an associated net loss of water and electrolytes.

Acid-Base Equilibrium↗
PubMed1975

Renal response to acid loading in the developing lamb fetus, intact in utero.

Response of the fetal kidney to metabolic acidosis was studied in five fetal lambs, 115-125 days gestation, in order to evaluate the renal contribution to elimination of hydrogen ion during intra-uterine development. Experiments were conducted on healthy unanesthetized fetuses, intact in utero, with catheters implanted at hysterotomy into a fetal femoral artery and vein and into the bladder via the urachus, four or more days prior to the study. A metabolic acidosis was induced by infusion of isotonic lactic acid, 15 m mole/kg, intravenously over a period of 90 minutes. Serial arterial samples were taken and urine collected in fractions before, during and for three hours following the infusion, for measurements of pH, bicarbonate, lactate and electrolytes as well as urine output. During the infusion, urine pH fell from 6.65 to 6.25 and was 6.34 three hours later (Figs. 1 to 4, Tabs. III to IV). Lactic acid infusion caused a prompt increase in urine output from a mean rate of 0.12 to a maximum of 0.28 ml/kg/min at the end of the infusion, returning to control rates three hours later. Lactate excretion increased from 0.05 to a maximum of 4.6 mumole/kg/min at the end of infusion; titratable acid increased from 0.22 to a maximum of 4 muEq/kg/min; the rates of excretion of lactate and titratable acid were still higher than control at the end of three hours. Ammonia excretion increased from 0.21 to a maximum of 0.56 muEq/kg/min three hours after the end of infusion. The acid infusion caused a small but significant fall in excretion of bicarbonate. During the 90 minutes of infusion and over the following three hours, about 800 mumole lactate was excreted while net acid excretion over the same period was no more than half that amount. The diuresis was also accompanied by a net loss of sodium and chloride, the excretion of these ions increasing more than threefold following acid infusion; excretion of potassium decreased to one-third its rate prior to the infusion. During the 90 minutes of infusion, blood pH fell from 7.36 to 7.13, base deficit rose from 3.8 to 16.4 mEq/L and lactate rose from 2.2 to 14.8 mM/L; there was also a small but significant rise in both blood PCO2 and PO2 (Figs. 1 to 2, Tabs. I to II). During the following three hours of recovery, pH rose gradually to 7.29, base deficit and lactate fell to 7.4 mEq/L and 8.7 mM/L respectively. Since renal excretion of net acid and lactate was small, the decrease in blood base deficit and lactate levels during the recovery must therefore be mainly due to equilibration in various fetal compartments as well as placental transfer. These experiments indicate that, in the lamb fetus, intact in utero, the kidney although limited by immaturity of several mechanisms, is capable of responding to an acid load and thus can make a small contribution to fetal homeostasis. The increase in excretion of net acid is accompanied by loss of sodium and chloride in the urine.

Acid-Base Equilibrium↗