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OBJECTIVE: We sought to determine whether a critical cardiac output and oxygen delivery exist in normal pregnancy. We also sought to determine the role of fetoplacental oxygen demand on maternal oxygen transport variables in response to decreased maternal cardiac output. STUDY DESIGN: We studied 10 adult female sheep, 5 nonpregnant and 5 pregnant. We placed a flow-directed thermodilution catheter in the pulmonary artery and a balloon-tipped catheter in the right atrium of the sheep. We also placed a catheter for pressure monitoring and blood sampling in the descending thoracic aorta in both the mother and fetus. We decreased maternal cardiac output by incremental inflation of the right atrial balloon. We measured maternal cardiac output by intravenous bolus thermodilution technique. We also measured maternal and fetal acid-base status and serum lactate concentrations. We calculated a variety of maternal cardiorespiratory variables, including systemic oxygen delivery, systemic oxygen consumption, and fractional whole body tissue oxygen extraction. RESULTS: The nonpregnant sheep displayed a critical cardiac output below which there was an abrupt decrease in oxygen consumption. In contrast, there was no critical level of cardiac output in the pregnant sheep. Maternal oxygen consumption was linearly dependent on cardiac output. Maximum fractional oxygen extraction was significantly lower in the pregnant sheep than in the nonpregnant sheep. CONCLUSION: States of low cardiac output in the pregnant sheep are associated with a lack of a critical cardiac output; the flow-dependent oxygen consumption observed is the result of either an impairment in tissue oxygen extraction or some degree of metabolic arrest or a combination of both. If this unique cardiac output - oxygen consumption relationship is seen in human pregnancy, it could have significant implications in the care of the critically ill obstetric patient. (Am J Obstet Gynecol 1996;175:222-8.)

Objective: The hypothesis of our study was that both the systemic and uteroplacental circulations would adapt to chronic maternal anemia to ensure that oxygen supply to maternal tissues would be adequate. Study Design: We measured cardiac output and uteroplacental blood flow and calculated systemic and uteroplacental oxygen delivery, extraction, and consumption in pregnant sheep that were anemic for 6 days (hematocrit 14%) and in normal sheep (hematocrit 28%). Results: When compared with normal pregnant sheep, anemic pregnant sheep had increases in cardiac output and uteroplacental blood flow, neither of which was sufficient to prevent systemic or uteroplacental oxygen delivery from decreasing. In spite of decreases in oxygen delivery, systemic and uteroplacental oxygen consumptions were maintained at normal levels because of increases in oxygen extraction. Conclusion: Maternal systemic and uteroplacental circulations are capable of adapting well to chronic maternal anemia.

The increased circulatory and metabolic demands of pregnancy lead to a variety of adaptive responses in many regional vascular beds. The concomitant development of anemia could modify these adaptive processes. The purpose of our studies was to quantify the regional vascular responses to chronic anemia in pregnant sheep and to compare those responses to those occurring with acute anemia. We measured regional blood flows and O2 deliveries and calculated vascular resistances in 10 near-term pregnant sheep, five of which were made anemic (hematocrit = 14%) for 6 days by isovolemic hemodilution with fresh plasma. The remaining five sheep served as controls (hematocrit = 28%). As a result of 6 days of anemia, almost all regional beds (except for the small intestines, colon, and spleen) had increases in blood flow, which helped maintain tissue O2 deliveries at or near normal levels. Tissues with increased flow accounted for 88% of cardiac output, in contrast to what has been reported for acute anemia of comparab...

We previously observed young lambs to be more tolerant of hypoxia; compared with older lambs, they accumulate lactate at a slower rate during comparable reduction in cardiac output, and have a greater percent decrease in cardiac output before onset of systemic lactate accumulation. To determine the mechanism of lactic acidosis and the cause for this "tolerance," we reduced cardiac output progressively in seven chronically catheterized conscious lambs (16.4 + 5.1 d) and measured hepatic and gastrointestinal (GI) blood flow (radioactive microspheres) and delivery, uptake, and extraction of lactate and O2. Hepatic O2 consumption declined proportionately below a critical hepatic O2 delivery (approximately 2 mL O2/min/kg), corresponding to the systemic O2 delivery associated with the onset of systemic lactate accumulation. As hepatic O2 delivery decreased below the critical value, there was initially net hepatic lactate uptake and then a change to net production when the O2 delivery decreased below approximately 1 mL O2/min kg. The GI tract had net lactate production at rest, but surprisingly switched to lactate uptake as cardiac output decreased. The mechanism of lactic acidosis was failure of hepatic lactate uptake to increase despite increased hepatic lactate delivery, as reported in adults subjects. However, in contrast, there was "true" hepatic dysfunction and lactate production only at the lowest levels of cardiac output, after onset of systemic lactate accumulation. Moreover, we speculate that tolerance of young lambs to hypoxia is at least due to two factors: 1) hepatic lactate uptake is maintained beyond the "critical" O2 delivery and fall in hepatic O2 consumption, and 2) there is a switch to lactate uptake by the GI tract serving to buffer the lactate.

Accurate assessment of gestational age and fetal weight in the pregnant ewe is important in both acute and longitudinal perinatal studies. We describe two morphometric methods based on the length of the fetal metatarsal bone. These measurements can be made intraoperatively or at postmortem. Metatarsal bone lengths can be used to better predict gestational age and fetal weight than previously described methods.

We chronically catheterized 15 newborn lambs (9.5 +/- 2.8 days) and measured the distribution of cardiac output by the radionuclide-microsphere technique at hematocrits ranging from 10 volumes % to 55 volumes %. Seven animals were made progressively anemic and eight polycythemic by means of exchange transfusions. Cardiac output and heart rate increased with decreasing hematocrit while whole body oxygen consumption showed a small decrease during severe anemia. Both cerebral and cardiac blood flow markedly increased during anemia which assured a relatively stable oxygen delivery to both organs. The changes seen for blood flow to the carcass (skin, bones, and muscle) were predictable from the effects of blood viscosity: small decreases in flow at the highest hematocrits and small increases in flow at the lowest hematocrits. Consequently, oxygen delivery was as low as 1 ml of oxygen/min/100 g at a hematocrit of 10 volumes %. Renal blood flow remained unchanged while oxygen delivery fell when hematocrit was decreased. Hepatic oxygenation was measured using a modification of the Fick principle. Hepatic blood flow showed only a small decrease as hematocrit increased and changed minimally during anemia resulting in a falling delivery of oxygen with anemia. A stable hepatic oxygen consumption was assured by a marked increase in oxygen extraction during anemia. Two differing organ responses to changes in hematocrit can be seen in the newborn: the brain and heart vary blood flow to assure an adequate delivery of oxygen while a number of other organs show less blood flow regulation and, most likely, vary oxygen removal from blood.(ABSTRACT TRUNCATED AT 250 WORDS)

We identified the effects of reductions in arterial blood oxygen concentration from 15.0 to 4.0 ml O2/dl blood on hepatic blood flow, oxygen delivery, oxygen consumption and oxygen extraction in nine chronically catheterized lambs, 9 +/- 1 (SD) days of age. Hypoxemia was induced by administering a gas mixture low in oxygen to the unanesthetized lambs. Hepatic blood flow was measured with the radioactive microsphere technique; hepatic oxygen delivery, extraction, and consumption were calculated with modifications of the Fick principle. When the lambs breathed room air, hepatic blood flow was 235 +/- 30 ml/min/100 gm (mean +/- SD); hepatic oxygen delivery, 24.6 +/- 3.0 ml O2/min/100 gm; oxygen extraction, 37 +/- 11%; and hepatic oxygen consumption, 8.9 +/- 1.9 ml O2/min/100 gm. As arterial blood oxygen concentration was reduced from 15 to 6.5 ml O2/dl blood, hepatic blood flow did not change. When the concentration was less than 6.5 ml O2/dl, hepatic blood flow decreased as a result of a decrease in portal blood flow. Hepatic oxygen delivery decreased in the whole range of arterial blood oxygen concentrations studied. Despite reductions in oxygen delivery of up to 50%, hepatic oxygen consumption did not fall because hepatic oxygen extraction increased as compensation. Oxygen consumption, however, was stable only when hepatic blood flow did not change in response to hypoxemia. When hepatic blood flow fell, hepatic oxygen consumption also fell. Our data indicate that hepatic oxygen requirements can be met during hypoxemia by increases in hepatic oxygen extraction as long as hepatic blood flow does not change. When hepatic blood flow falls, hepatic oxygen consumption decreases even though oxygen reserves are still present. These data indicate that hepatic oxygenation in the neonate, as in the adult, is dependent on stable hepatic perfusion rather than adequate oxygen supply.

To determine whether the high oxygen affinity of fetal blood, compared with that of the adult, is advantageous to the fetus during fetal anemia we studied 16 chronically catheterized fetal lambs. Half of the lambs had hemoglobin-oxygen affinity reduced acutely by isovolemic exchange transfusion with fresh adult whole blood; the other half served as controls. In both groups of fetuses, we measured fetal oxygen delivery, oxygen consumption, and acid-base state at normal fetal hematocrit levels and during reductions in the hematocrit level of 30% (moderate anemia) and 60% (severe anemia) produced by isovolemic exchange transfusions with plasma. At normal fetal hematocrit levels, reductions in hemoglobin-oxygen affinity had no effect on fetal oxygen consumption or acid-base state. During moderate anemia, fetal oxygen delivery decreased in both series of fetuses, but oxygen consumption and base excess fell only in those fetuses whose circulations contained adult hemoglobin. During severe anemia, oxygen consumption and base excess decreased in both groups of fetuses, although these changes were more pronounced in fetuses with adult hemoglobin than in those with fetal hemoglobin. Our data indicate that, even though a high hemoglobin-oxygen affinity may not be essential to a healthy fetus, it is critical for normal metabolism in a fetus subjected to a hypoxic stress such as anemia.

In 11 chronically catheterized fetal lambs (123 +/- 6, mean +/- SD, days of gestation; term = 147 days), we measured fetal oxygen delivery and oxygen consumption before and during reductions in umbilical blood flow (Qumb). Qumb was reduced by inflation of a balloon occluder located just proximal to the origin of the common umbilical artery. Measurements were made while the unanesthetized maternal sheep received either room air or 100% oxygen to breathe. In oxygen-treated fetuses, oxygen concentrations in umbilical venous blood (Cuvo2) and arterial blood (Cao2) were increased over a wide range of Qumb when compared with those of room air-treated fetuses. Because of these responses, fetal oxygen delivery (Do2 = Qumb X Cuvo2) and oxygen consumption [Vo2 = Qumb(Cuvo2-Cao2)] were greater in oxygen-treated fetuses than in room air-treated fetuses during episodes of reduced Qumb. In oxygen-treated fetuses, Vo2 decreased from normal levels only when Qumb was less than or equal to 75 ml/min/kg of fetus, whereas in room air-treated fetuses Vo2 decreased at Qumb less than or equal to 150 ml/min/kg. Our data indicate that oxygen administration to the pregnant sheep increases oxygen delivery to the fetus during times of reduced umbilical perfusion and that this supplemental oxygen supply provides an oxygen reserve with which the fetus can maintain oxidative metabolism. These data may be relevant to those clinical conditions, such as umbilical cord compression in labor, that are associated with reductions in umbilical blood flow.

The effects of dexamethasone on maternal and fetal hemodynamic states and fetal oxygenation were determined in chronically instrumented unanesthetized pregnant ewes and fetal lambs. Intravenous injections of pharmacologic doses of dexamethasone to the mother failed to alter maternal blood pressure, heart rate, blood flow in the uterine artery supplying the pregnant horn, or uterine vascular resistance. Direct administration of dexamethasone to the fetus had no effect on fetal blood pressure, heart rate, acid-base state, or oxygenation. Furthermore, direct fetal administration of dexamethasone did not produce premature parturition.

Preterm labor is responsible for a majority of cases of perinatal morbidity and deaths. Prevention of preterm labor is not usually possible; thus pharmacologic treatment is the only recourse available. Numerous agents have been used to treat preterm labor, but none has proved to be superior. This report reviews the current information available about the pharmacology of labor-inhibiting drugs and discusses the clinical approach to the management of preterm labor.

In 101 diabetic pregnant women (Classes A through D) 146 determinations of the lecithin/sphingomyelin ( L/S ) ratio were carried out. Gestational ages were verified by serial fetal cephalometry. No L/S ratios of more than 2.0 were found before 341/2 weeks' gestation; however, in 42 per cent of patients the L/S ratio was below 2.0 at 36 weeks' gestation or later. Respiratory distress syndrome (RDS) was found in 16 neonates of women with L/S ratios of 2.0 or higher; however, RDS incidence varied depending on the mode of delivery. Abdominal delivery was performed before 37 weeks' gestation in 19 patients with L/S ratios of 2.0 or higher and resulted in neonates with RDS in 41 per cent of cases. Vaginal delivery was accomplished before 37 weeks' gestation in 10 patients with L/S ratios of 2.0 or higher and no subsequent neonatal RDS was observed. After 37 weeks' gestation neonatal RDS is rare, irrespective of mode of delivery. The data presented suggest that similar numerical values of the L/S ratio at different gestational ages have a different predictive value for the occurrence of neonatal RDS.

Changes in the distribution of portal venous blood flow to the left and right lobes of the liver and through the ductus venosus were determined from before birth through 9 days of age in 25 chronically catheterized fetal and newborn lambs. Blood flow distribution was calculated by means of the radionuclide-labeled microsphere technique. With umbilical cord clamping portal venous blood flow distribution to the right lobe of the liver decreased when compared to that in the term fetus; distribution to the left lobe and ductus venosus increased. More than 50% of portal blood flow was shunted through the ductus venosus during the first hour after birth. Ductus venosus shunts of at least 25% of total portal blood flow were noted in half the lambs between the second and sixth days of life. Portal venous distribution to the right lobe was inversely related to the fraction of portal blood flow shunted through the ductus venosus. The ratio of right lobe weight to total liver weight was significantly correlated with the ratio of right lobe flow to total liver flow (r = 0.73; P less than 0.001). The conclusion is that large and persistent ductus venosus shunts are normal during the first postnatal week in lambs.

Perinatal outcome and obstetric practices during 1970 and 1977 were compared. None of the 6,740 fetuses delivered with birth weights of 1,000 gm or greater in 1970 had electronic fetal monitoring (EFM). In 1977, 5,987 of 8,174 fetuses delivered had EFM (72.7%). High-risk factors were significantly more frequent in the pregnant patient population in 1977. The incidence of intrapartum stillbirths and severe birth asphyxia was significantly lower in 1977. These reductions remained significant when corrected for changes in obstetric practices other than EFM as well as for changes in patient population. The neonatal death rate was not significantly changed. The primary cesarean section rate increased from 4.4% to 10.1%, mostly because of a greater number of cesarean sections done for failure to progress in labor and breech presentation. Only 15% of the overall increase in cesarean section rate was because of a greater frequency of the indication of fetal distress. The incidence of severe birth asphyxia was the same among the unmonitored patients in 1970 and 1977. In 1977, however, the monitored patients had a significantly lower incidence of severe birth asphyxia than the unmonitored patients.

Betamethasone was administered to six rhesus-sensitized pregnant women carrying seven fetuses in an attempt to accelerate fetal pulmonary maturation. A reduction in optical density of amniotic fluid at 450 mμ was observed in all cases following steroid therapy; however, only minimal changes were noted in the lecithin-sphingomyelin ratio. The implications of these findings for the management of rhesus-sensitized pregnancies are discussed.

SUMMARY We evaluated the circulation of the liver and ductus venosus, using the radionuclide-labeled mkrosphere technique, in 24 chronically prepared fetal lambs. We placed catheters in fetal descending aorta and inferior vena cava, and hi a carotid artery and an umbilical vein; in 11 fetuses, we aho Inserted a catheter hi a mesenteric vein that drained into the portal vein. After allowing 2-4 days for recovery from the stresses of anesthesia and operation, we measured blood flow to the fetal liver and hs various lobes and through the ductus venosus. Total Mood flow to the liver was 435 ± 122 ml/min per 100 g liver (mean ± SD), of which hepatic arterial flow represented 9%, portal venous flow 18%, and umbilical venous flow 73%. Hepatic arterial and umbilical venous flows were approximately equally divided between left and right lobes, although portal blood flow was directed almost exclusively to the right lobe. The right lobe received 40% more total blood flow than the left, even though the left lobe weighed more than the right. Approximately 53% of umbilical venous blood flow but less than 9% of portal venous blood flow entered the ductus venosus; umbilical venous flow therefore accounted for more than 98% of ductus venosus blood flow. Ductus venosus flow showed a strong linear correlation with umbilical blood flow. However, there was no relationship between ductus venosus flow and gestational age. The results suggest that the liver receives a large Mood flow primarily because of a large umbilical venous contribution. It is not dear whether the fetal liver requires this large flow and peculiar lobar distribution for normal function and growth. It is unlikely, however, that the ductus venosus functions actively to maintain a stable blood flow to the fetal liver. THE LIVER of the fetus receives its blood supply from the hepatic artery, portal vein, and umbilical vein. Total blood flow to the fetal liver must be high, because a large umbilical venous blood flow passes through the liver. Nevertheless, the actual flow that reaches the liver from all three vascular sources has not been measured previously. The relative contributions of hepatic arterial and portal and umbilical venous blood flows to the various lobes of the liver also have not been studied quantitatively. Anatomically, the left lobe of the liver is supplied by branches of the umbilical vein, while the right lobe is supplied by portal venous branches 11 (Fig. 1). Except for occasional small branches, no umbilical blood vessels extend into the right lobe, and no portal blood vessels reach the left lobe. Branches of the hepatic artery supply both lobes, but arterial flow to the whole liver is small.

We studied the vascular reactivity of the systemic and uterine circulations of six pregnant sheep. We placed catheters in a maternal carotid artery and a jugular vein, and then implanted an electromagnetic flow transducer around the uterine artery of the pregnant horn. After allowing 3 days for recovery from anesthesia and operation, we measured mean arterial blood pressure, heart rate, uterine blood flow, and calculated uterine vascular resistance, then separately infused angiotensin and norepinephrine in each ewe at the rate that produced a 20 torr pressor response. Dexamethasone, 0.2 mg. per kilogram of body weight, was then injected intravenously daily for 2 to 4 days. On the day following the final injection of dexamethasone, we separately infused angiotensin and norepinephrine at a rate that, before steroid treatment, produced a 20 torr pressor response. Administration of dexamethasone for 2 to 4 days did not change mean arterial blood pressure, heart rate, uterine blood flow, or uterine vascular resistance. Prior to steroid treatment, angiotensin increased blood pressure, decreased heart rate, but had no consistent effect on uterine blood flow or uterine vascular resistance; norepinephrine increased blood pressure without chenging heart rate, decreased uterine blood flow, and increased uterine vascular resistance. The changes produced by angiotensin and norepinephrine were the same after dexamethasone treatment. These studies indicate that dexamethasone does not influence systemic and uterine vascular reactivity during normal sheep pregnancy.

In adult nonpregnant animals and human beings, glucocorticosteroids increase circulating leukocytes (predominantly neutrophils) and decrease lymphocytes, monocytes, and eosinophils. We were interested in studying effects of glucocorticoids on leukocyte counts during pregnancy to determine any differences between responses in the nonpregnant and pregnant states. After general anesthesia was administered, we placed catheters in a carotid artery and a jugular vein in pregnant sheep and in fetal lambs. Six days after surgery, we administered dexamethasone intravenously to the mother (0.2 mg. per kilogram) or to the fetus (0.06 mg. per kilogram) and obtained maternal and fetal jugular venous blood samples immediately before (control) and 3, 6, 12, 24, 48, and 72 hours after steroid injection. administration of dexamethasone to the mother significantly increased total leukocyte and neutrophil counts (leukocytes per cubic millimeter blood) and decreased lymphocyte and eosinophil counts, but it did not change monocyte counts. Leukocyte counts returmed to control values within 48 hours. Administration of dexamsthasone to the fetus rapidly increased total leukocyte and neutrophil counts, decreased monocyte and eosinophil counts, and had no effect on lymphocyte counts. Fetal leukocyte counts returned to control values by 24 hours after dexamethasone injection. Our results suggest that maternal and fetal leukocytes can respond to glucocorticoids as they do in the adult nonpregnant state.

We evaluated the effects of alterations in fetal hematocrit on fetal oxygenation in 10 chronically catheterized fetal lambs. Hematocrit was varied from 10% to 55% by slow isovolemic exchange transfusions with plasma or packed red blood cells obtained freshly from donor fetuses. At each hematocrit studied, we measured umbilical blood flow (Qumb) and the oxygen concentrations in umbilical venous blood (CUVO2) and arterial blood (CAO2) and calculated fetal oxygen delivery (Qumb X CUVO2), oxygen extraction [(CUVO2 - CAO2)/CUVO2], and oxygen consumption [Qumb (CUVO2 - CAO2)]. Fetal oxygen delivery was maximal at a fetal hematocrit of 33% (mean oxygen delivery = 23 ml of oxygen per minute per kilogram of fetus) and decreased as hematocrit was raised or lowered from that value. Despite these reductions in oxygen delivery, fetal oxygen consumption was relatively stable (at about 7 ml of oxygen per minute per kilogram) at hematocrits ranging from about 16% to 48% because of compensatory increases in fetal oxygen extraction. Regardless of whether oxygen delivery decreased because of anemia or polycythemia, fetal oxygen consumption was maintained as long as oxygen delivery was greater than about 14 ml of oxygen per minute per kilogram of fetus. When oxygen delivery was less than 14 ml of oxygen per minute per kilogram, fetal oxygen consumption fell while arterial blood base deficit increased, indicating that oxygen supply was inadequate for fetal oxygen demands. These results indicate that fetal aerobic metabolism can be sustained over a wide range of fetal hematocrits. Furthermore, our data support the concept that the level of fetal oxygen delivery is an important determinant of the adequacy of fetal oxygenation.

We measured regional blood flows and cardiac output and calculated regional oxygen deliveries (blood flow X arterial blood oxygen concentration) and systemic oxygen delivery, oxygen extraction, and oxygen consumption as maternal hematocrit was varied randomly between 31% and 8% by exchange transfusion with plasma or packed sheep red blood cells. We observed three patterns of response: In the heart, brain, and adrenal glands, oxygen delivery was constant or nearly constant over the range of hematocrits studied; in the kidneys, splanchnic organs, and uteroplacental tissues, oxygen delivery was a linear function of hematocrit; in the carcass tissues, oxygen delivery decreased slowly as hematocrits were reduced from 31% to 15% and dropped rapidly at hematocrits less than or equal to 15%. Systemic oxygen consumption was maintained at normal levels, despite reductions in hematocrit to about 15%, because oxygen extraction increased as compensation. At lower hematocrits, systemic oxygen consumption fell in association with a metabolic acidemia, suggesting that, with this severity of acute anemia, oxygen supply to some tissues in the pregnant sheep was inadequate for tissue metabolic demands.

We studied the effects of acute isovolemic maternal anemia on several variables of uterine and fetal oxygenation to answer these two questions: (1) Does maternal anemia cause reductions in oxygen delivery to the uterus, placenta, and fetus? (2) If so, what is the impact of such reductions on fetal oxidative metabolism? In 15 chronically catheterized pregnant sheep and fetal lambs, we measured uterine and umbilical blood flows and uterine and fetal oxygen deliveries, oxygen extractions, and oxygen consumptions at various, randomly selected maternal hematocrits ranging from 30% to 8%. We altered maternal hematocrit by performing isovolemic exchange transfusions with plasma or packed red blood cells. Uterine and umbilical blood flows were measured with the radionuclide-labeled microsphere technique, and the variables of oxygenation were calculated with modifications of the Fick principle. Decreases in maternal hematocrit led to linear reductions in oxygen delivery to the uterus, placenta, and fetus. Despite reductions in oxygen delivery of up to 50%, fetal oxygen consumption was maintained, because of compensatory increases in oxygen extraction. When hematocrit (and thus fetal oxygen delivery) was reduced by more than 50%, fetal oxygen consumption and the arterial blood base excess both decreased, indicating that, at these hematocrit levels, the supply of oxygen to fetal tissues was inadequate for the demands for oxygen by these tissues.

The purpose of our experiments was to relate blood flow and oxygen delivery (blood flow x arterial blood oxygen concentration) to fetal organs as functions of fetal hematocrit. In 12 chronically catheterized fetal lambs, we observed two patterns of responses of fetal organs and tissues to isovolemic alterations in fetal hematocrit from 12% to 55%. In group 1 organs (brain, heart, adrenal glands), blood flows increased as hematocrit was either raised or lowered from normal such that oxygen delivery to these organs was stable over the entire range of hematocrits studied. In group 2 organs (gastrointestinal tract organs, spleen, kidneys, placenta, and carcass), blood flows varied little over the range of hematocrits from 12% to 40% or 45% but decreased at hematocrits greater than or equal to 40% to 45%. Because of these flow responses, oxygen delivery to these organs and tissues was maximal at hematocrits ranging from 32% to 38%. Our data indicate that the various organs of the unanesthetized fetal lamb respond in different ways to alterations in hematocrit. It is of particular interest that, in the great majority of the organs of the fetus, oxygen delivery is maximal at hematocrits considered normal for the fetal lamb in utero.

In nine chronically catheterized fetal lambs (120 to 135 days; term 147 days), umbilical venous blood flow and its distribution were measured by the radionuclide-labeled microsphere technique before and during autonomic blockade with atropine (0.20 to 0.25 mg/kg; seven studies) or phentolamine (0.10 to 0.12 mg/kg; six studies). Atropine significantly increased mean fetal heart rate (182 to 207 beats/min), descending aortic blood pressure (49 to 55 mm Hg), and umbilical venous blood flow (210 to 239 ml/min/kg fetus), without changing umbilical venous blood pressure. Phentolamine decreased mean descending aortic pressure (48 to 45 mm Hg), but did not affect heart rate, umbilical venous blood pressure, or umbilical venous blood flow. Neither atropine nor phentolamine altered the distribution of umbilical venous blood flow to the ductus venousus, the liver, or the other fetal organs. These data indicate that the cholinergic nervous system only indirectly affects the basal umbilical venous blood flow in the near-term fetal lamb. This effect is small and is secondary to associated changes in heart rate and arterial blood pressure. Neither the cholinergic nor the α-adrenergic systems influence the basal distribution of umbilical venous blood flow.

Ninety-two women in preterm labor were randomly assigned to receive either terbutaline or ethanol. In women with intact membranes, terbutaline was significantly more effective than ethanol in preventing progressive cervical dilation during the first 36 hours of treatment while betamethasone was given to the mother. Additionally, pregnancy was maintained significantly longer in women with intact membranes who were treated with terbutaline (15 ± 4 days) rather than with ethanol (10 ± 3 days). However, only 18% of women in each treatment group maintained their pregnancy beyond 36 weeks’ gestation. In women with ruptured membranes and cervical dilation less than 4 cm, terbutaline was significantly better than ethanol in maintaining pregnancy for a minimum of 36 hours. Serious maternal side effects were not observed with terbutaline or ethanol, although a majority of women also received betamethasone. Neither drug caused serious adverse neonatal effects.

We determined hepatic arterial (QHA) and portal venous (Qpv) blood flows and calculated, utilizing the Fick principle, net hepatic glucose production (PGLUC), O2 delivery (DO2), O2 consumption (VO2), and O2 extraction (VO2/DO2), in 7 chronically catheterized lambs (9-15 d). Studies were done with the lambs fasted and at 1, 2, 3, 4, and 6 hr postprandially. We measured O2 contents (Lex-O2-Con), blood flows (radioactive microspheres), and glucose (glucose oxidase). The table indicates mean results. (* = significantly different from fasting) Our results show that the VO2 of the neonatal liver decreases postprandially. This decreased VO2 is associated with a decreased O2 extraction rather than a decrease in DO2 or hepatic blood flow. Since glucose production is increasing at a time when hepatic oxygen consumption is decreasing, these data indicate that hepatic metabolism shifts postprandially to less oxygen-dependent processes.