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Biomedical subjects

L S James

Publications and source records attributed to L S James.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1978

Determination of fetal lung maturity by fluorescence polarization of amniotic fluid.

The degree of fluorescence polarization (P value) of 1,6-diphenyl-1,3,5-hexatriene has been shown to be an excellent indicator of the lecithin/sphingomyelin (L/S) ratio in laboratory prepared liposomal dispersions. In order to test the validity of this technique in amniotic fluid, the L/S ratio and P value of 161 amniotic fluid specimens were determined. In 127 the P value was less than or equal to 0.336 and the L/S ratio was greater than or equal to 2. In 26 the P value was greater than 0.336 and the L/S ratio was less than 2 (P less than 0.05). The amniotic fluid P value is affected by blood or meconium but not by surgical lubricants or bilirubin. We concluded that the degree of fluorescence polarization of amniotic fluid indicates fetal lung maturity as reliably as the L/S ratio. However, this method has important technical and practical advantages that make it more applicable for a clinical laboratory.

Amniotic Fluid↗
PubMed1978

Maternal ABO blood group type B: a risk factor in the developement of neonatal group B streptococcal disease.

In a prospective study of maternal genital colonization with group B streptococci (GBS) at the time of delivery, epidemiological data, including blood type (ABO group), were recorded for the 1,062 patients studied. Blood type B was found in a statistically significant higher proportion of patients colonized with GBS (28%) compared with the total population (16.4%) (P less than .005, X2 = 8.43). Women with blood type B were twice as likely to be colonized as those with types O or A. Hypotheses to explain this observation include the possibilities that GBS possess a B-like antigen, rendering parturients who lack anti-B antibody at increased risk for GBS colonization, or that GBS possess a receptor site for B surface antigens. One may speculate that a mutation toward an affinity for the human ABO blood group type B accounts for the advent of the group B Streptococcus as a significant perinatal pathogen.

ABO Blood-Group System↗
PubMed1977

Temperature gradient between fetus and mother as an index for assessing intrauterine fetal condition.

Temperature gradient between fetus and mother (deltaTF-M) was measured in 29 pregnant baboons. Thermocouples were implanted in the fetal esophagus and the maternal colon, and, in some instances, thermistor probes were also placed in the fetal esophagus, scalp, and shoulder muscle. Under steady-state conditions, the fetal temperature was found to be higher than that of the mother. Temperatures in the fetal esophagus, scalp, and shoulder were 0.47, 0.28, and 0.19 degrees C. respectively, higher than those in the maternal colon. There was an increase in deltaTF-M during acute fetal stress induced by asphyxia, secondary to occlusion of the umbilical cord, maternal aorta, or inferior vena cava, or to acutely increased uterine activity. This increase in deltaTF-M most likely reflects impairment of heat dissipation from the fetus to the maternal compartment. A decreased deltaTF-M was observed when the stress on the fetus was subacute and prolonged. This is probably the result of a diminution of heat production by the fetus as the metabolic rate is lowered during prolonged hypoxia. Ten to 30 minutes after the cessation of vital signs of the fetus, the deltaTF-M became zero.

Acute Disease↗
PubMed1977

High vasopressin concentrations in human umbilical cord blood--lack of correlation with stress.

Marked elevations in the vasopressin concentrations in human umbilical cord blood have been reported previously (4, 8). This could either be a part of generalized increase in the activity of fetal endocrine system at the time of birth, a phenomenon that has led to the concept of fetal participation in the onset of labor, or simply due to the stress of delivery. The present study is an attempt to examine the later possibility. Plasma vasopressin was determined by radioimmunoassay [9] in separately collected arterial and venous blood from the umbilical cords of 24 babies spontaneously delivered and 14 babies born after Caesarian Section in the absence of labor. Arterial acid-base determinations were done in each case. The Apgar Score was evaluated by one individual. In order to obtain a general idea of circulating concentration of this hormone in the neonatal period, vasopressin concentrations were determined in the systemic venous blood of 12 normal and 10 stressed babies. Vasopressin concentrations in the umbilical arterial blood of babies born after spontaneous delivery were remarkably high, as compared to all the other groups. Despite a wide range, between 5-2200 pg/ml, there was no correlation between the magnitude of vasopressin elevation and the severity of fetal asphyxia (Fig. 1). The present finding in part, confirms and expands previously observed increased vasopressin levels in the cord blood after spontaneous vaginal delivery. In addition, a lack of correlation between fetal asphyxia and the vasopressin levels suggests that these high levels may not be related to this form of stress.

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↗
PubMed1976

Prolonged infusion of diazoxide in the management of premature labor in the baboon.

The management of premature labor by the prolonged infusion of diazoxide was evaluated in 33 pregnant baboons. The drug was administered intravenously to the mother with an average rate of 0.065 mg/kg/min for 4 hours. Mild to moderate spontaneous labors were significantly inhibited by diazoxide without jeopardizing the fetus. Diazoxide produced a significant increase in maternal heart rate, but its effect on fetal circulation was minimal. Fetal acid-base state and arterial oxygenation remained essentially unchanged throughout the period of observation. Intravenous administration of this drug to the fetuses caused only mild cardiovascular changes irrespective of its preexisting conditions. Thus, a slow intravenous infusion of diazoxide to the mother in a low dosage appears to be of value for inhibiting the uterine activity in early labor, without interfering with the fetal well-being.

Amniotic Fluid↗
PubMed1976

The effect of diazoxide on uterine blood flow in pregnant sheep.

Diazoxide, a labor inhibiting agent, was administered intravenously at various rates to seven pregnant, near-term sheep to evaluate its effect on cardiovascular and uterine hemodynamics. Uterine blood flow was measured with electromagnetic flow transducers. Rapid administration of diazoxide resulted in a profound maternal tachycardia with hypotension, an increase in uterine vascular resistance, and a significant decrease in uterine blood flow. With slow infusion of the drug, the changes in heart rate and blood pressure were minimized, uterine vascular resistance was decreased, and uterine blood flow was maintained. Therefore, slow infusion appears to be the preferred method for inhibiting labor with diazoxide.

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

Transfer of lidocaine across the sheep placenta to the fetus. Hemodynamic and acid-base responses of the fetal lamb.

Placental transfer of lidocaine administered to pregnant sheep and removal of the drug from the fetal circulation were determined. Responses of the hemodynamic and acid-base state in the mother and fetus were also studied. Lidocaine readily crossed the placenta and appeared in the fetal blood as early as one minute following injection. Disappearance of lidocaine in the asphyxiated fetus tended to be slower than in the normal one. Lidocaine produced a transient fall in the fetal heart rate which was accompanied by a decrease in blood pH and oxygenation. Lidocaine also reduced umbilical blood flow and, in some instances, uterine blood flow. Decrease in umbilical blood flow was more pronounced in the initially asphyxiated fetus.

Acid-Base Equilibrium↗
PubMed1975

Myocardial conduction defects in association with compression of the umbilical cord. Experimental observations on fetal baboons.

Experiments have been performed in 16 pregnant baboons to study in greater detail the fetal hemodynamics, heart rate, and acid-base changes during occlusion of the umbilical cord. A total of 32 observations were made during which the umbilical cord was completely occluded with the fetus intact in utero; 11 were made after the intravenous administration of atropine, 0.01 to 0.02 mg. per kilogram, to fetus. Various degrees of conduction defects occurred in 17 of 21 observations before atropine. Complete atrioventricular block with extrasystoles was seen six times. Upon release of cord occlusion, there was a rapid recovery of myocardial conduction. Atropine prevented myocardial conduction defects; bradycardia was less and the onset was delayed. These observations suggest that myocardial conduction defects which occur during the course of cord occlusion are due to parasynpathetic stimulation. They could also be due to an increased sensitivity of the fetal myocardium to acetylcholine under hypoxic conditions. No recommendation can be made at the present time with regard to the administration of atropine to the fetus when cord compression is suspected on clinical grounds.

Acid-Base Equilibrium↗