Search PubMed⌕ Search

Biomedical subjects

S S Daniel

Publications and source records attributed to S S Daniel.

At least 55 records · Page 3Linked to original sources
PubMed1981

Release of vasopressin by the fetal lamb during premature parturition induced with corticotropin.

These studies were implemented to assess the relationship between fetal vasopressin secretion and the progression of parturition as well as the contribution of specific stimuli to vasopressin release during labor. In chronically catheterized fetal lamb preparations, labor was induced by infusion of adrenocorticotropin (12.5 mg/kg/hr) to seven fetuses at 130 +/- 1 day of gestation. Before labor, fetal plasma vasopressin concentrations were 2.1 +/- 1.4 pg/ml and remained low (5.3 +/- 3.4 pg/ml) during prodromal and early phases of labor, but rose significantly in the active and expulsive phases (39.6 +/- 27.5 and 173.3 +/- 152.9 pg/ml) to reach peak values at delivery (584.2 +/- 433 pg/ml) and decrease by 30 min after birth (359.8 +/- 90.0 pg/ml). At delivery, fetal plasma vasopressin concentrations were strongly correlated (P less than 0.001) with hormone values obtained during the latter phases of labor. Fetal arterial pH and oxygen tension was inversely correlated with plasma vasopressin (P less than 0.01). No similar correlations were found with arterial PCO2, K, Na, Cl, osmolality, or packed cell volume. Unexpectedly, we observed a significant (P less than 0.001) and progressive decrease in fetal oxygen tension during the induction process. Other characteristics of adrenocorticotropin-induced parturition seemed to mimic those of spontaneous labor.

Adrenocorticotropic Hormone↗
PubMed1981

Postnatal adjustment in renal function.

Renal function was studied serially in 17 healthy term infants during the hours immediately following birth. Of 14 infants delivered vaginally eight received placental blood transfusion and six did not. The remaining three infants were delivered by cesarean section and received placental blood transfusion. Results indicate that the general pattern of change in urine output (V), clearance of inulin (CIN), and p-aminohippuric acid (CPAH), was similar in all infants despite a wide range in each of the functions measured. The pattern showed an initial increase in V, CIN, and CPAH followed by a decline to low values in all infants by 3 hours of age. Urine osmolality and output generally changed in opposite directions. During the first hour the values for V ranged from 0.02 to 0.47 ml/min; for CIN, from 0.5 to 9.1 ml/min; for CPAH, from 1.4 to 21.8 ml/min; and for osmolality, from 98 to 457 mOsm/kg. By 4 hours of age the values for V ranged from 0.01 to 0.15 ml/min; for CIN, from 0.8 to 3.7 ml/min; for CPAH, from 0.8 to 7.5 ml/min; and for osmolality, from 240 to 520 mOsm/kg. The initial values of V, CIN, and CPAH, as well as the changes, were greatest in those infants who received a placental transfusion; however, there were no statistical differences among the means of the various groups. By 4 hours of age, the range of values observed in the initial measurement was much less pronounced. This probably reflects the achievement of stability of renal circulation following adaptation to a variety of stresses during the intrapartum period.

Adaptation, Physiological↗
PubMed1981

Response to rapid volume expansion during the postnatal period.

This study was designed to test the hypothesis that the postnatal diuresis observed in healthy neonates during the second hour of life is due to an expansion of their extracellular volume as a result of a purposeful or spontaneous placental blood transfusion. Seven healthy infants were given infusions of a 5% glucose solution, 0.3 to 2.5 ml/kg/min, over a period of 14 to 70 minutes during the third or fourth hour of life. Plasma and urine were analyzed for osmolality, inulin, and p-aminohippuric acid in order to estimate osmolal and free water clearances as well as glomerular filtration rate and renal plasma flow. Despite individual variation in initial values and in response, glucose infusion caused a prompt two- to fourfold increase in urine output with a similar increase in glomerular filtration rate and renal plasma flow but no consistent change in urine osmolality. The response was of short duration, subsiding within less than 30 minutes following the end of infusion. The fraction of exogenous fluid load excreted was less than 5% in five of seven infants. This study indicates that during the first few hours of postnatal life, the kidney of the newborn infant is capable of responding to a water load in a fashion similar to the kidney of the neonate aged a few days. It can also be concluded that the transient postnatal diuresis observed in these infants could, in part, be due to the expansion of extracellular volume by placental blood transfusion.

Blood Volume↗
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↗