Biomedical subjects

C A Gleason

Publications and source records attributed to C A Gleason.

At least 19 recordsLinked to original sources

PubMed1995

Reinnervation of the rat bladder with a somatic nerve and a striated muscle flap.

PURPOSE: Current techniques of ventral sacral root stimulation to regain voluntary motor control of the decentralized urinary bladder depend upon intact parasympathetic innervation of the detrusor. We investigated techniques that might allow restoration of motor control of the bladder after efferent parasympathetic impairment. MATERIALS AND METHODS: In a chronic rat model, we evaluated whether motor control of a peripherally denervated bladder could be restored by transplantation of autologous excitable tissues and subsequent electrostimulation. Either a somatic nerve or a striated muscle flap was used as the transplant. RESULTS: Four months after the initial surgery, electrostimulation of the somatic nerve implant provoked bladder contractions--a response that was blocked by atropine. Stimulation of the nerve innervating the striated muscle flap also provoked bladder contractions; these were not affected by atropine and were slightly reduced by hexamethonium. CONCLUSION: Reinnervation of the bladder with somatic nerves or striated muscles is possible in principle. Future experiments will clarify the clinical significance of electrostimulation of such implants.

Animals↗

PubMed1992

The effect of magnetic resonance imagers on implanted neurostimulators.

This in-vitro study was designed to investigate the safety of various implanted neurostimulators in magnetic resonance (MR) imagers. The effects of the static and changing magnetic fields and the radio frequency (RF) electromagnetic field generated by 0.35 and 1.5 T MR imagers on the voltage output of four models of implantable passive neurostimulators and two models of implantable self-powered neurostimulators was studied. The neurostimulators were mounted on a support and placed in the imagers. An oscilloscope monitored the voltages at the outputs of the neurostimulators. For an Avery single-channel stimulator, located at the isocenter, the amplitude of the output pulses induced by the 0.35 T imager was 6V; from a 1.5 T imager, it was 12 V. These amplitudes can cause discomfort and possible harm to a patient if the typical therapeutic value is 1-5 V. The amplitude of the stimulator receiver's output decreased to relatively safe values beyond 40 cm from the isocenter. By contrast, there was no significant voltage output from the Medtronic SE-4 receiver. For two models of self-powered neurostimulators, the Medtronic Itrel and the Cordis MK II, the programmed stimulus parameters were not affected by the pulsed magnetic fields of the MR imagers. However, the RF fields at the isocenter heated the metal case of the stimulators. The rotational and linear forces produced by the fixed magnet on the Cordis MK II were judged to be too strong for a patient with this implant to be scanned. The study showed that patients with certain types of implanted neurostimulators can be scanned safely under certain conditions.

Electric Stimulation Therapy↗

PubMed1992

Cerebral responses to acute maternal alcohol intoxication in immature fetal sheep.

Previous studies in mature fetal sheep have shown that alcohol depresses cerebral blood flow (CBF), cerebral O2 consumption (CMRO2), and cerebral glucose consumption (CMRglu). This effect earlier in gestation might contribute to the pathogenesis of fetal alcohol syndrome. Physiologic studies of immature fetal sheep have demonstrated lower CBF, CMRO2, and CMRglu as well as a blunted vasodilatory response to hypoxia compared with mature fetal sheep. The purpose of this study was to determine whether immature fetal responses to alcohol are blunted compared with near-term fetal responses. We studied seven immature fetal sheep in utero at 92 +/- 1 d gestation (term = 147 d) 2 d after placement of vascular catheters. Pure ethanol (1 g/kg) was infused i.v. to the mother over 1 h. We measured CBF and myocardial blood flow by radioactive microspheres and calculated CMRO2 and CMRglu using arterial and sagittal sinus O2 and glucose concentrations. At a fetal ethanol concentration of 33 + 8 mmol/L (150 +/- 37 mg/dL), there were no significant changes in CBF, CMRO2, or CMRglu. There was mild hypoglycemia (glucose concentration = 1.05 +/- 0.2 versus 1.33 +/- 0.2 mM baseline) and lactic acidemia (lactate concentration = 1.29 +/- 0.3 versus 1.07 +/- 0.2 mM baseline). Cardiovascular variables were unchanged as was myocardial blood flow. The immature fetal sheep brain shows no significant cerebrovascular and metabolic response to acute alcohol intoxication compared with mature fetal sheep. Mild hypoglycemia and lactic acidemia did develop. The reason for the developmental differences in response to alcohol and their relationship to fetal alcohol syndrome remain to be elucidated.

Alcoholic Intoxication↗

PubMed1991

Control of the transition from sensory detection to sensory awareness in man by the duration of a thalamic stimulus. The cerebral 'time-on' factor.

A 'time-on' theory to explain the cerebral distinction between conscious and unconscious mental functions proposes that a substantial minimum duration ('time-on') of appropriate neuronal activations up to about 0.5 s is required to elicit conscious sensory experience, but that durations distinctly below that minimum can mediate sensory detection without awareness. A direct experimental test of this proposal is reported here. Stimuli (72 pulses/s) above and below such minimum train durations (0-750 ms) were delivered to the ventrobasal thalamus via electrodes chronically implanted for the therapeutic control of intractable pain. Detection was measured by the subject's forced choice as to stimulus delivery in one of two intervals, regardless of any presence or absence of sensory awareness. Subjects also indicated their awareness level of any stimulus-induced sensation in each and every trial. The results show (1) that detection (correct greater than 50%) occurred even with stimulus durations too brief to elicit awareness, and (2) that to move from mere detection to even an uncertain and often questionable sensory awareness required a significantly larger additional duration of pulses. Thus simply increasing duration ('time-on') of the same repetitive inputs to cerebral cortex can convert an unconscious cognitive mental function (detection without awareness) to a conscious one (detection with awareness).

Awareness↗

PubMed1990

Effect of acute hypoxemia on brain blood flow and oxygen metabolism in immature fetal sheep.

Studies of cerebral blood flow and oxygen metabolism during acute hypoxic hypoxia in fetal sheep have been confined to late gestation, a time when brain development in this species is largely complete. There is no systematic study of cerebral vascular responses to acute hypoxic hypoxia in immature fetal sheep or, indeed, in immature brains of any species. We studied 13 fetal sheep in utero at 93 +/- 1 days gestation (term = 145-150 days), 48 h after intravascular catheters were placed into the superior sagittal sinus, axillary arteries, and inferior vena cava. We measured brain blood flow by the microsphere method. Cerebral oxygen consumption was calculated with the use of blood flow to the cerebral hemispheres (cerebrum, diencephalon, mesencephalon) and arterial and sagittal sinus values for oxygen content. Fractional oxygen extraction was calculated as the ratio between oxygen consumption and oxygen transport. We altered fetal oxygenation by changing the mother's inspired oxygen concentration. As in the near-term fetus, acute hypoxic hypoxia resulted in increased blood flow to cerebral hemispheres, cerebellum, and pons-medulla; furthermore, the increase in blood flow was sufficient to sustain cerebral oxygen consumption. However, in contrast to near-term fetuses, the increase in blood flow to the cerebral hemispheres was not sufficient to maintain convective oxygen transport. Cerebral oxygen consumption was therefore sustained in part by an increase in fractional extraction. Blunted hypoxic vasodilation in immature fetuses might reflect either immature regulatory mechanisms or an inability of cerebral vessels to respond to the usual stimuli. It is also possible that hypoxic vasodilation was blunted by reflex stimulation of the sympathetic nervous system.

Acute Disease↗

PubMed1990

Effect of extracorporeal membrane oxygenation on cerebral blood flow and cerebral oxygen metabolism in newborn sheep.

Extracorporeal membrane oxygenation (ECMO) supplies respiratory support to term or near-term infants with respiratory failure. Although infants requiring this therapy may have already sustained significant hypoxia and/or ischemia predisposing them to neurologic injury, the high incidence of neuroimaging abnormalities in the ECMO population raises concerns about the additional neurologic risk associated with the ECMO procedure itself. Our study was undertaken to evaluate the effects of ECMO on the normal neonatal cerebral circulation. Thirteen newborn lambs (1-7 d of age) were placed on normothermic venoarterial ECMO using a silicone membrane oxygenator and roller occlusion pump. Regional brain blood flows, cerebral oxygen consumption, fractional oxygen extraction, and oxygen transport were determined 30 and 120 min after initiation of ECMO. Neither cerebral blood flow (baseline, 60.2 +/- 23.6; 30 min, 56.1 +/- 18.1; 120 min 56.1 +/- 12.9 mL/100 g/min) nor oxygen metabolism (cerebral oxygen consumption: baseline, 4.48 +/- 1.48; 30 min, 3.86 +/- 1.53; 120 min, 4.10 +/- 1.32 mL/100 g/min and oxygen extraction: baseline, 0.52 +/- 0.09; 30 min, 0.47 +/- 0.14; 120 min, 0.46 +/- 0.14 mL/100 g/min) changed after the initiation of ECMO. Regional and left/right blood flow differences were not noted. These findings suggest that in healthy newborn lambs, initiation of ECMO does not alter cerebral blood flow or oxygen metabolism.

Animals↗

PubMed1989

Cerebral blood flow and metabolism during and after prolonged hypocapnia in newborn lambs.

We studied the effects of prolonged (6 hours) hypocapnia and the abrupt termination thereof on cerebral blood flow and metabolism in six paralyzed, sedated (but not anesthetized) newborn lambs. Thirty minutes after institution of hyperventilation to an arterial carbon dioxide pressure of 15 +/- 2 torr, hyperventilation, cerebral blood flow had returned to baseline. Abrupt termination of hyperventilation after 6 hours resulted in a 110 +/- 71% increase in cerebral blood flow over baseline after 30 minutes of normocapnia. This cerebral hyperemia persisted for at least 90 minutes after hyperventilation was discontinued. Cerebral oxygen consumption did not change throughout the study. The posthypocapnia hyperemia noted in these animals after abrupt normalization of arterial carbon dioxide pressure may contribute to the increased risk of intracranial hemorrhage in newborn infants who are treated similarly in the management of pulmonary hypertension.

Animals↗

PubMed1989

Cerebral blood flow, oxygenation, and carbohydrate metabolism in immature fetal sheep in utero.

Studies of cerebral blood flow (CBF) and metabolism in fetal sheep have been largely confined to late gestation, a time when brain development in this species is largely complete. Few studies have been done at a time when the fetal sheep brain is in the midst of rapid differentiation and development. We studied seven fetal sheep in utero at 91 days of gestation (term = 145-150 days) 24 h after catheters were placed into the sagittal sinus, axillary artery, and inferior vena cava. We measured CBF by the microsphere method and used arteriovenous differences of O2, lactate, and glucose to calculate cerebral O2 consumption (CMRo2), fractional O2 extraction, glucose consumption, O2-glucose index (OGI), and cerebral lactate production. Compared with near-term fetal sheep, we found lower CBF (33.9 +/- 5.3 ml.100 g-1.min-1), lower glucose consumption (8.5 +/- 1.25 mumol.100 g-1.min-1), and lower CMRo2 (41.8 +/- 8.8 mumol.100 g-1.min-1). Fractional O2 extraction was 0.29 +/- 0.04, which is similar to near-term fetal sheep. There was consistent cerebral lactate production (2.45 +/- 1.58 mumol.100 g-1.min-1). The OGI was 81 +/- 16%, i.e., oxidative metabolism could account for 81% of glucose uptake. Lactate production accounts for virtually all glucose uptake exceeding that required for oxidation.

Animals↗

PubMed1989

Relationship of diaphragmatic contractility to diaphragmatic blood flow in newborn lambs.

We determined the relationship of diaphragmatic contraction rate to diaphragmatic blood flow (Qdi), metabolism, and contractility in nine open-chested mechanically ventilated newborn lambs. The diaphragm was paced for 15 min at slow (20/min) and fast (100/min) contraction rates each followed by a 30-min rest period. There was a mild reduction in transdiaphragmatic pressure (Pdi) during the slow contraction period accompanied by a shift to the right of the curve relating stimulation frequency (10-100 Hz) to Pdi. Pdi returned to control at the start of the fast contraction period, but then fell by 30% within 2 min with continued fast contraction rates. The frequency-Pdi curve was significantly shifted to the right. Qdi, O2 transport, and O2 consumption increased during slow contraction and to an even greater extent during fast contraction. Fractional O2 extraction reached an apparent maximum during slow contraction. Lactate efflux from the right phrenic vein during slow contraction remained unchanged from control. During fast contraction lactate efflux rose proportionately more than did O2 consumption. We conclude that the energy demands at fast rates of diaphragmatic contraction in newborn lambs cannot be met by aerobic metabolism alone despite increasing O2 transport to the diaphragm.

Animals↗

PubMed1989

Stimulation of locus coeruleus in man. Preliminary trials for spasticity and epilepsy.

Stimulating electrodes were chronically implanted unilaterally (in 1975-1977) in the vicinity of the locus coeruleus (LC) in three patients, one with cerebral palsy-spastic quadriplegia, two with epilepsy (one grand mal, one psychomotor). Effective excitation of efferent LC axons was indicated by measuring rises in 3-methoxy-4-hydroxyphenylethyleneglycol in the jugular and systemic venous blood following a 6-min stimulus with discontinuous bursts of pulses. There was a substantial reduction of spasticity during and after stimulation. Improvement was verified by double-blind failures of the stimulator, and the stimulus therapy is still in use after 9 years. There appeared to be a reduction in incidence and severity of both types of epileptic seizures, although this was not rigorously established. The patient with psychomotor epilepsy reported a considerable lengthening of preseizure auras (to 15-30 min), an unusual number of which terminated without a seizure.

Adolescent↗

PubMed1989

Cerebral and peripheral circulatory responses to intracranial hypertension in fetal sheep.

Fetal head compression during normal labor can increase intracranial pressure (ICP). We studied the cerebral and peripheral blood flow responses to ICP elevation in utero in chronically catheterized fetal sheep using the radiolabeled microsphere technique. ICP was elevated, stepwise, in increments of 6 +/- 1 mm Hg by infusion of artificial cerebrospinal fluid into a lateral ventricle. When ICP was raised to within 28 mm Hg of baseline mean arterial blood pressure (i.e., ICP above 22 mm Hg), arterial pressure began to increase. Above this ICP level, up to 41 mm Hg, mean cerebral perfusion pressure was maintained by equivalent increases in arterial pressure. Cerebral blood flow and O2 uptake at the highest ICP levels were not different from baseline values. Changes in peripheral organ blood flow were graded according to the level of ICP. At the highest level (ICP = 41 mm Hg), renal, gastrointestinal, and skin blood flow decreased by 68%, 69%, and 65%, respectively. Myocardial and adrenal blood flow doubled, whereas heart rate and cardiac output were unchanged. Placental blood flow increased in proportion to arterial pressure. Arterial plasma epinephrine, norepinephrine and arginine vasopressin increased by nearly two orders of magnitude. Therefore, as ICP approaches baseline mean arterial pressure, fetal lambs are capable of sustaining cerebral perfusion by initiating profound visceral vasoconstriction without curtailing placental blood flow. Since cerebral O2 uptake was maintained, there is no evidence that stimulation of the peripheral response requires pronounced cerebral ischemia. This highly developed Cushing response may be important for ensuring cerebral viability when the fetal head is compressed during parturition.

Animals↗

PubMed1988

Fetal cerebral responses to ventilation and oxygenation in utero.

Previous studies have shown that cerebral oxygen consumption (CMRO2) increases by nearly 50% at birth. The perinatal factors responsible for this increase are unknown; however, one possibility is that fetal CMRO2 is constrained by the normal intrauterine arterial PO2 (PaO2) of approximately 20 mmHg. We investigated this possibility in seven near-term chronically instrumented fetal sheep (131-138 days gestation) in which we inserted vascular catheters and an endotracheal tube. After 1-3 days recovery, we measured cerebral blood flow (CBF) with radiolabeled microspheres and calculated CMRO2. Measurements were made in utero under three conditions for each fetus: 1) nonventilated control; 2) ventilation with 3% O2-5% CO2-92% N2; and 3) ventilation with an inspired oxygen concentration sufficient to raise fetal PaO2 to normal newborn levels (mean 73 mmHg). A calf lung surfactant extract (CLSE) was instilled into the endotracheal tube of the fetus before ventilation to ensure adequate levels of alveolar surfactant and to maintain stable pH and arterial PCO2. The results showed that increasing fetal arterial PO2 to postnatal levels did not consistently increase CMRO2. CBF decreased as arterial O2 content (CaO2) rose, with an inverse hyperbolic response similar to that previously found to relate CBF to CaO2 during fetal hypoxic hypoxia. This indicates that the normally low intrauterine PaO2 does not intrinsically limit CMRO2 and implies that the rapid increase in CMRO2 at birth reflects the activation of specific cellular and physiological processes at (or near) this unique developmental event.

Animals↗

PubMed1988

Indomethacin and patent ductus arteriosus: effects on renal function in preterm lambs.

To examine the independent effects of a patent ductus arteriosus and of indomethacin therapy on the renal function of the preterm newborn, we created a preterm lamb model in which ductus diameter could be regulated. We studied 24 preterm newborn lambs. Eight lambs (group 1) had their ductus closed at delivery and received no indomethacin. Eight lambs (group 2) had their ductus closed and then received indomethacin (0.3 mg/kg) at 5.5 h; eight lambs (group 3) had their ductus kept open and then received indomethacin at 5.5 h. Hemodynamic and renal function measurements were made at 5 h (pretreatment) and at 12.5 h. In group 2 lambs there was a significant reduction in inulin clearance (GFR) and osmolal clearance after indomethacin. In contrast, lambs with an open ductus (group 3), when compared with lambs with a closed ductus (groups 1 and 2) at 5 h, already had significantly decreased blood pressure, GFR, urine volume, and osmolal clearance. Following indomethacin treatment, group 3 lambs showed no further decrease in renal function. We suggest that in preterm lambs with patent ductus, the apparent lack of renal dysfunction following indomethacin treatment reflects underlying diminished renal function.

Animals↗

PubMed1987

Prostaglandins and the developing kidney.

Prostaglandins PGE2, PGD2, PGI2, and PGF2 alpha, as well as thromboxanes and leukotrienes, are synthesized by the fetal and neonatal kidney. The major prostaglandin, PGE2, PGD2, and PGI2, increase RBF, free water clearance, urine flow, and natriuresis. Alterations in the synthetic and catabolic activity of renal prostaglandins with advancing gestational and postnatal age occur along with concomitant alterations in RBF, GFR, and water and electrolyte excretion, suggesting that the prostaglandins play an important role in renal functional development. Indomethacin treatment may affect both fetal and neonatal renal function. Long-term maternal indomethacin treatment may decrease fetal urine output enough to alter amniotic fluid volume. Neonatal indomethacin therapy may cause transient dose-related renal dysfunction characterized by a decrease in urine output, but this renal dysfunction also depends in part on dosage, timing of therapy, and the cardiovascular and renal status of the infant prior to treatment. New areas of research interest include urinary prostaglandins as a marker for development of essential hypertension, and the possible interaction between antenatal steroids and renal function in the newborn.

Animals↗

PubMed1986

Oxygenation does not stimulate hepatic gluconeogenesis in fetal lambs.

We have previously shown that the healthy fetal lamb liver does not release glucose and does not demonstrate gluconeogenesis. Shortly after birth, however, the liver releases glucose both by glycogenolysis and by gluconeogenesis. Previously it has been suggested that increased oxygen availability stimulates hepatic gluconeogenesis at birth. To test this hypothesis, we increased fetal arterial blood pO2 by ventilating the fetus with high oxygen gas mixtures in utero. We placed intravascular catheters in the right or left hepatic vein, umbilical vein, inferior vena cava, and descending aorta and inserted a large polyvinyl tube into the trachea of seven fetal lambs at 134 +/- 2.2 days gestation. Studies were done several days after surgery. 14C-lactate was infused intravenously and 14C-glucose concentrations were measured in hepatic venous and umbilical venous blood during a control period, during ventilation with 5% CO2, 3% O2, 92% N2, and then during ventilation with 5% CO2 and 95% O2. The difference between these two measurements represented hepatic gluconeogenesis. Arterial blood glucose concentrations and blood gases were also measured during each study period. Ventilation with 3% O2 did not significantly change arterial PO2 but ventilation with 95% oxygen increased mean arterial pO2 from a control of 16.7 to 156.3 torr. Mean arterial blood glucose concentration increased significantly from a control of 11.9 to 17.6 mg/dl during ventilation with 3% O2 and to 19.1 mg/dl during ventilation with 95% O2. However, the hepatic-umbilical venous 14C-glucose concentration difference was not significant when control values were compared with each ventilation period. We conclude that an acute increase in fetal oxygenation does not stimulate hepatic gluconeogenesis in near-term fetal lambs.

Animals↗

PubMed1985

Hepatic oxygen consumption, lactate uptake, and glucose production in neonatal lambs.

Previous studies have evaluated neonatal hepatic metabolism in vitro, and neonatal hepatic oxygen consumption has been measured in vivo, but direct measurements of neonatal hepatic metabolism have not been reported. We studied seven neonatal lambs at age 7-10 days after placing catheters chronically in the hepatic vein, portal vein, descending aorta, left ventricle, and inferior vena cava. Hepatic blood flow was measured by the radioactive microsphere technique. Oxygen consumption and glucose and lactate fluxes were measured using the Fick principle. 14C-lactate was infused intravenously and lactate and glucose specific activities were measured and used to calculate hepatic gluconeogenesis from lactate. Neonatal hepatic blood flow was 254.5 +/- 50.3 ml/min/100 g (mean +/- SD) with 5.4 +/- 4.6% from the hepatic artery and 94.6 +/- 4.6% from the portal vein. Hepatic oxygen consumption was 7.2 +/- 2.4 ml/min/100 g and oxygen extraction was 44.9 +/- 15.4%. Oxygen extraction correlated inversely with oxygen delivery. In the seven lambs, there was net hepatic lactate uptake of 10.2 +/- 5.0 mg/min/100 g (1.13 +/- 0.56 mM) and hepatic glucose production of 30.8 +/- 11.3 mg/min/100 g (1.71 +/- 0.62 mM). In the five lambs in which hepatic gluconeogenesis was measured, 12.4 +/- 5 mg (1.37 +/- 0.56 mM) of lactate was converted to glucose per 100 g liver, accounting for 38.4% of the hepatic glucose production in these lambs. Blood flow and oxygen and substrate delivery to the neonatal liver are lower than those to the fetal liver but the neonatal liver extracts more oxygen and substrates and is able to produce glucose by gluconeogenesis from lactate.

Animals↗

PubMed1985

Lactate uptake by the fetal sheep liver.

Lactate is produced by the sheep placenta and is an important metabolic substrate for fetal sheep. However, lactate uptake and release by the fetal liver have not been assessed directly. We measured lactate flux across the liver in 16 fetal sheep at 129 (120-138) days gestation that had catheters chronically maintained in the fetal descending aorta, inferior vena cava, right or left hepatic vein, and umbilical vein. Lactate and hemoglobin concentrations and oxygen saturation were measured in blood drawn from all vessels. Umbilical venous, portal venous, and hepatic blood flow were measured by injecting radionuclide-labeled microspheres into the umbilical vein while obtaining a reference sample from the descending aorta. We found net hepatic uptake of lactate (5.0 +/- 4.4 mg/min per 100 g liver). A large quantity of lactate was delivered to the liver (94.2 +/- 78.1 mg/min per 100 g), so that the hepatic extraction of lactate was only 7.7 +/- 6.5%. Hepatic oxygen consumption was 3.18 +/- 3.3 ml/min per 100 g, and the hepatic lactate/oxygen quotient was 2.07 +/- 1.54. There was no significant correlation between hepatic lactate uptake and hepatic lactate or glucose delivery, hepatic oxygen consumption, hepatic blood flow, hepatic glucose flux, total body oxygen consumption, arterial pH, oxygen content, or oxygen saturation. There was, however, a significant correlation between hepatic lactate uptake and umbilical lactate uptake (r = 0.74, P less than 0.005) such that net hepatic lactate uptake was nearly equivalent to that produced across the umbilical-placental circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Gluconeogenesis by the fetal sheep liver in vivo.

Hepatic gluconeogenesis is an important source of glucose postnatally. Whether hepatic gluconeogenesis contributes to fetal glucose supply has not been studied directly in vivo. Previous studies of gluconeogenesis in fetal sheep have assessed total fetal glucose production, and the results have been controversial. To assess the specific role of the liver in gluconeogenesis in fetal sheep, we placed catheters in the right or left hepatic vein, umbilical vein and the inferior vena cava of six fetal sheep (mean gestational age 134 days) and infused a radioactive gluconeogenic substrate (14C-lactate or 14C-alanine) into the fetal inferior vena cava. We measured 14C-glucose radioactivity (dpm/ml) in the right or left hepatic vein and calculated the arteriovenous difference in 14C-glucose radioactivity (dpm/ml) across the right or left liver lobe. We found that only 0.35% of the 14C substrates perfusing either the right or the left hepatic lobe of the fetal liver were converted to 14C-glucose. Even when considerable glucose was released by the liver, the percentage of substrates converted to glucose remained very low (maximum 1.7%), indicating that gluconeogenesis did not contribute significantly to the glucose released. We conclude that gluconeogenesis by the fetal liver contributes negligibly to the glucose supply in fetal sheep.

Alanine↗