Precision Microwave Spectroscopy of the Positronium 2

We report the results of a new measurement of the positronium 2 ^{3}S_{1}→2 ^{3}P_{2} (ν_{2}) interval. Using a modified experimental arrangement we have significantly reduced the effects of microwave reflections, which in previous experiments resulted in shifts and asymmetric line shapes. With the improved apparatus we obtain an experimental value of ν_{2}=8627.94±0.95 MHz, which is within 1.3σ of the theoretical value 8626.71±0.08 MHz.

Effect of intravenous cocaine on uterine blood flow in the gravid baboon.

Cocaine abuse during pregnancy is associated with adverse perinatal outcome, believed to be a result of potent vasoconstrictive effects that cocaine has on the maternal cardiovascular system. The direct effect of cocaine on the pregnant, nonhuman primates' uterine vasculature in vivo has not been examined. We investigated the effects of intravenous cocaine on maternal arterial blood pressure, uterine blood flow, and uterine vascular resistance in four unanesthetized, chronically instrumented pregnant baboons. Baboons were instrumented during the latter half of pregnancy, placing an ultrasonic flow probe around one uterine artery and catheters in the maternal inferior vena cava and aorta. Bolus intravenous cocaine hydrochloride doses of 0.05 mg/kg, 0.1 mg/kg, and 0.3 mg/kg by maternal weight were infused 30 minutes apart at least 5 days after surgical instrumentation. The maternal blood pressure rose 7.3% and 12.0% after the 0.1 mg/kg and 0.3 mg/kg cocaine infusions, respectively, and the uterine blood flow fell in a dose-dependent fashion 13.1% and 22.7%. Plasma norepinephrine levels rose in response to the 0.3 mg/kg cocaine infusion. These studies show that low doses of cocaine significantly reduce uterine blood flow in the pregnant baboon in a dose-dependent manner by increasing uterine vascular resistance.

Fetal and newborn lambs differ in their cardiopulmonary responsiveness to adenosine agonists.

We investigated cardiorespiratory responses to adenosine analogs in the pre- and postnatal periods in an unanesthetized chronic animal preparation. Heart rate, blood pressure, breathing movements and blood gases were measured in 8 fetal lambs (117-130 days gestation) and 9 newborn lambs (4-30 days). Various doses of analogs were given by intravenous infusion. L-N6-5'-Phenylisopropyladenosine (L-PIA), 5-N-ethyl carboxamidoadenosine (NECA) and cyclohexyladenosine (CHA) were studied. All analogs produced dose-dependent bradycardia and hypotension in the fetus. However, in the newborn, NECA produced a dose-dependent tachycardia, whereas PIA and CHA produced a dose-dependent bradycardia. Fetal breathing movements were interrupted by all the analogs, but they did not produce apnea in the newborn. No changes in blood gases were observed. The actions of the adenosine agonists were blocked by caffeine.

Anti-Ata causing mild hemolytic disease of the newborn.

We report here a case of moderately severe hemolytic disease of the newborn (HDN) due to anti-Ata. The gravida 5 proposita was group A rr and previously was found to have anti-Ata and -D. At the 35-week mark of this pregnancy, her anti-Ata demonstrated a titer of 256, score 79. Fluid obtained by amniocentesis at 36 weeks showed an optical density at 450 nm of 0.08 (midzone). The baby was delivered at 38 weeks by cesarean section. The cord cells were group A rr with a 3+ direct antiglobulin test. The dichloromethane eluate of the infant's cells demonstrated anti-Ata specificity only. At birth, the infant's total bilirubin (TB) was 2.1 mg per dl and the hematocrit level (Hct) was 33.8 percent. Within 8 hours, the TB had risen to 3.8 mg per dl. Phototherapy was initiated at 7-1/2 hours and maintained for 40 hours. The infant's TB rose to a maximum level of 10.5 mg per dl 24 hours after phototherapy was discontinued. At discharge 4 days postpartum, the infant's TB had dropped to 9.2 mg per dl, and the Hct value was 38 percent. On a visit 7 days postpartum, the infant's TB level had fallen to 6.5 mg per dl and the hct value was 38 percent. Transfusions were not necessary.

Phenyl isopropyl adenosine alters fetal electrocorticogram, breathing and heart rate.

Six fetal sheep were equipped with intratracheal, amniotic and vascular catheters and electrocorticogram electrodes to study the effect of phenyl isopropyl adenosine (PIA) on electrocorticogram and fetal breathing movements. Three animals had functioning electrocardiogram electrodes. During 1,000-min control periods, low-voltage high-frequency (LVHF) electrocorticogram predominated 60 +/- 1% (mean +/- SEM) of total time. Fetal breathing movements occurred 34 +/- 1% of total time and only during LVHF electrocorticogram. PIA 0.125 mg was given intravenously to the fetus during established LVHF electrocorticogram and fetal breathing movements. LVHF electrocorticogram converted in 58 +/- 16 s to high-voltage low-frequency (HVLF) electrocorticogram which persisted for 10 +/- 3 min. This was followed by a third electrocorticogram pattern for 119 +/- 12 min. Fetal breathing movements ceased in 47 +/- 25 s and did not recur for 150 +/- 20 min. An increase in fetal breathing movements (59 +/- 2% of total time) occurred between 300 and 800 min (control 34 +/- 1%, p less than 0.05). Electrocardiogram demonstrated a decrease in heart rate from 170 +/- 6 to 90 +/- 6 beats per min with return to baseline in 113 +/- 49 min. No significant changes occurred in blood gases. We conclude that fetal electrocorticogram, fetal breathing movements and heart rate are influenced by adenosine.

Effect of hypocalcemia on cardiac function in very-low-birth-weight preterm neonates: studies of blood ionized calcium, echocardiography, and cardiac effect of intravenous calcium therapy.

Traditionally, in infants, a serum calcium value less than 7.0 mg/dL is considered to impair cardiac function. In very-low-birth-weight infants, we studied the hypotheses that decline in serum calcium to 6.0 mg/dL (1) would not impair cardiac function and (2) ionized calcium would remain greater than 3.0 mg/dL. We also evaluated the effect of calcium infusion on cardiac function. We studied 15 normokalemic and normonatremic infants whose birth weights were 822 to 1,450 g and were less than 32 weeks' gestation. When serum calcium declined to less than 6.0 mg/dL, 18 mg/kg of calcium as 5% calcium gluconate was infused for 10 minutes. Serum total calcium concentration, blood ionized calcium concentration, ECG, and M-mode echocardiogram were obtained on entry into the study, when the infants were hypocalcemic, immediately after treatment with calcium, and eight hours after treatment. Ionized calcium values were calculated based on serum total calcium and serum protein, and corrected calcium values were calculated based on serum total calcium, serum albumin, and blood pH. In all infants, serum calcium value declined to less than 7.0 and in eight infants to less than 6.0 mg/dL. Assessment of heart rate, systolic blood pressure, ejection fraction, left ventricular systolic time interval, right ventricular systolic time interval, fiber shortening index, and left ventricular mean velocity of circumferential fiber shortening showed no significant alteration from baseline during hypocalcemia or in association with intravenous slow bolus infusion of 18 mg/kg of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of morphine on fetal electrocortical activity and breathing movements in fetal sheep.

Morphine (1 mg/kg) given to the lamb fetus near term induces a significant increase in low-voltage high-frequency (LVHF) electrical activity in the brain. This pattern of the electrocorticogram (ECOG) is associated with simultaneous continuous fetal breathing movements of greater amplitude than control. Naloxone prevents and reverses these morphine-induced changes. The observed phenomena suggest that opiate receptors may play a stimulant role in the control of fetal LVHF ECOG and fetal breathing movements.

Morphine stimulates rapid, regular, deep, and sustained breathing efforts in fetal lambs.

We gave morphine (1-4 mg) to 11 unanesthetized lamb fetuses at 123-141 days of gestation. After a delay of 28 +/- 7 min (mean +/- SE), the fetuses began forceful, frequent, regular, and sustained inspiratory efforts lasting continuously for 105 +/- 15 min and continuing intermittently for a total of 155 +/- 13 min. The induced breathing motions are more forceful, frequent, and regular than the naturally occurring efforts of the fetus and resemble neonatal breathing motions. The phenomenon is blocked by 0.5 mg of naloxone but not by 0.1 mg of atropine. We conclude that the mechanism of action involves the opiate receptor system. We speculate that endorphins may have a role in the regulation of breathing in the fetal and newborn lamb.

Retinal and choroidal blood flow in unstressed fetal and neonatal lambs.

The relationship between retinal blood flow (RBF) and choroidal blood flow (ChBF) and the oxygen content of arterial blood was investigated in 12 fetal lambs. The postnatal changes in these flows were studied in twelve newborn lambs. RBF and ChBF were determined by means of radioactive microspheres 3 to 10 days after implantation of the injection and sampling catheters. Fetal blood flows were measured at different levels of oxygenation. The postnatal flows were measured while the lamb breathed room air. The fetal data suggest an inverse relationship between RBF and arterial oxygen content. Concomitant changes in fetal ChBF were unrelated to arterial oxygen content. Because of the inverse relationship between RBF and arterial oxygen content, the product of RBF and arterial oxygen content was independent of the state of fetal oxygenation. RBF did not change with birth, whereas ChBF increased. There was no change in RBF with postnatal age whereas ChBF decreased significantly with increasing age.

Induction of fetal breathing by metabolic acidemia and its effect on blood flow to the respiratory muscles.

Sustained and vigorous fetal breathing activity was produced in a chronic fetal lamb preparation by infusion into the fetus of either NH4Cl or HCl. Over a 2 to 3 hour period, 20 to 25 mEq/kg were infused. All of the fetuses tolerated blood pH values of 6.7 to 6.8 and survived. The breathing activity began after the completion of the infusion, and consisted of regular 30 to 50 torr inspirations at a rate of 60 to 120 breaths/min. This activity was continuous for as much as 8 hours, and persisted with pauses and decreased amplitude for 24 to 36 hours. During fetal breathing, blood flow to the diaphragm and intercostal muscles increased approximately 12- and sixfold, respectively.

Redistribution of cardiac output and oxygen delivery in the hypoxemic fetal lamb.

In hypoxia, fetal cardiac output and the product arterial O2 content x blood flow to the fetal heart and central nervous system (CNS) tend to remain constant. As a consequence the percentage of cardiac output directed to the heart and CNS increases hyperbolically in inverse relation to the oxygen content of the fetal ascending aorta, [O2]as. The fetal lamb maintains [O2]as approximately 0.45 mM (0.45 +/- 0.02 SEM) higher than the O2 content in the abdominal aorta, [O2]ab, over a wide range of oxygenation. When [O2]as decreases below the 2 mM level, the [O2]as--[O2]ab difference (delta O2) decreases also. A mathematical model of the fetal circulation shows that delta O2 is a function of the ratio oxygen consumption of fetal upper body/abdominal aorta blood flow (VU/FA). The behavior of delta O2 in hypoxia can be explained by assuming that the VU/FA ratio is maintained in moderate hypoxia and decreases in sever hypoxia.

Blood flow to fetal organs as a function of arterial oxygen content.

In a sheep preparation the blood flow to fetal organs was studied 3 to 10 days after surgery by means of the microsphere technique over a range of fetal arterial O2 content from 6 to 1 mM. Blood flows to neural tissues (cerebrum, cerebellum, brain stem), heart, and the adrenals increased in inverse relation to arterial O2 content. As a result the arterial supply of O2 to these organs tended to remain constant over the O2 range studied. Blood flow to the fetal lungs decreased progressively with hypoxia. The blood flow to kidneys, digestive tract, pancreas, and carcass had a tendency to remain constant or increase gradually in the transition from high to moderately low levels of arterial O2 content and then to decrease abruptly in more severe hypoxia. Umbilical blood flow did not change systematically in relation to arterial O2 content.

Regulation of cerebral blood flow in the ovine fetus.

The effects on fetal cerebral blood flow (Qc) of changes in the carotid arterial and sagittal sinus venous PO2, PCO2, and oxygen content were studied in the chronically catheterized ovine fetus in utero at 130-140 days of gestation. Forty-seven measurements of Qc were made in 20 fetuses with radioactive microspheres. In 11 of these animals, 84 measurements of cerebral arteriovenous differences of oxygen content were performed, permitting an indirect measurement of cerebral blood flow (Qc*), assuming a constant cerebral metabolic rate. Arterial and, in 11 animals, sagittal sinus blood was withdrawn for analysis of PO2, PCO2, oxygen content, and pH at the time of the flow measurements. Preliminary analysis showed the best predictor of Qc and Qc* to be the reciprocal of the arterial oxygen content (1/CaO2). Multiple linear regression analysis combining the effects of 1/CaO2 with arterial PCO2 (PaCO2) gave the following equations: Qc = 458.8 (1/CaO2) + 2.68 PaCO2 - 107.93 (R2 = 0.68); Qc* = 435.54 (1CaO2) + 2.20 PaCO2 - 75.03 (R2 = 0.86). As a result of the hyperbolic relationship between Qc (and Qc*) and CaO2, changes in CaO2 at the low levels found during intrauterine life exert an important influence on the fetal cerebral circulation.

Fetal cerebral oxygen consumption at different levels of oxygenation.

Cerebral oxygen consumption (VCO2) was measured in 10 unanesthetized, chronically catheterized fetal sheep at 130-140 days of gestation. The VCO2 was calculated using cerebral blood flow (QC) measured with radioactive microspheres and the cerebral arteriovenous difference of O2 content (C(a-V)O2) calculated from preductal arterial and sagittal sinus venous blood. The ewe was exposed to varying concentrations of oxygen, resulting in fetal arterial oxygen contents (CaO2) of 0.89-5.58 mM, arterial oxygen tension (PaO2) values of 14-36 Torr, and cerebral venous oxygen tension (PVO2) values of 9-25 Torr. Although there was a clear relationship between the fetal CaO2 and C(a-V)O2, this was shown to be the result of changes in Qc rather than changes in VCO2. There was not a statistically significant correlation between either CaO2 or PVO2 and VCO2 over this range of oxygenation. On the other hand, C(a-V)O2 was highly correlated with Qc. There is no evidence that VCO2 is a function of oxygen tension (PO2) in the unanesthetized fetal sheep as long as the sagittal sinus PO2 is greater than or equal to 9 Torr.