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PubMed1991

Colfosceril palmitate. A review of the therapeutic efficacy and clinical tolerability of a synthetic surfactant preparation (Exosurf Neonatal) in neonatal respiratory distress syndrome.

Colfosceril palmitate (dipalmitoylphosphatidylcholine) is the primary surface-active agent of natural lung surfactant and the major constituent of exogenous surface replacement preparations. Exogenous surfactants derived from either natural (i.e. animal and human) or synthetic sources are indicated for the prophylaxis and treatment of neonatal respiratory distress syndrome. One of the synthetic surfactants, Exosurf Neonatal, is the focus of this review. This preparation is composed of colfosceril palmitate plus cetyl alcohol and tyloxapol, which facilitate rapid spreading and adsorption of the surface-active agent at the air-alveolar interface. For review purposes, this preparation is referred to only as colfosceril palmitate. Comparative trials with air placebo have shown that colfosceril palmitate improves clinical outcome in infants weighing greater than 700g at birth by reducing mortality and increasing the number of infants who survive without bronchopulmonary dysplasia. It also reduces the number of deaths from respiratory distress syndrome and decreases the incidence of air leak events such as pulmonary interstitial emphysema and pneumothorax. Although colfosceril palmitate itself is very well tolerated and does not increase the incidence of most complications of prematurity or of respiratory distress syndrome, its use is associated with a higher incidence of apnoea of prematurity and pulmonary haemorrhage compared with air placebo, possibly because of earlier extubation of surfactant-treated infants following an improved clinical course and decreased pulmonary vascular resistance secondary to improved ventilation, respectively. Colfosceril palmitate thus has an established efficacy in the prophylaxis and treatment of premature infants with respiratory distress syndrome. Ongoing trials may identify whether prophylactic or rescue administration of the surfactant preparation is the preferred approach and whether different dosage regimens or different administration techniques impart greater therapeutic efficacy. Importantly, it also remains to be determined whether any of the available surfactant preparations, including Exosurf Neonatal, will provide distinct therapeutic advantages over the others.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1994

Economic outcomes of colfosceril palmitate rescue therapy in infants weighing 1250g or more with respiratory distress syndrome: results from a randomised trial.

An analysis of the economic data from a multicentre, randomised, placebo-controlled clinical trial of colfosceril palmitate in infants with neonatal respiratory distress syndrome (NRDS) and birthweights of 1250g or more is presented. Two 5 ml/kg (67.5 mg/kg) doses of a synthetic surfactant (colfosceril palmitate) or air placebo were administered to 1237 infants who were receiving mechanical ventilation and had an arterial/alveolar oxygen tension ratio of less than 0.22. In addition to the clinical end-points for safety and efficacy, data were collected on length of hospital stay, days in the neonatal intensive care unit, days on mechanical ventilation, days on oxygen, and hospital charges until the child reached 1-year adjusted age. One-year adjusted age is attained when the time elapsed since birth is equal to 365 days plus the number of days of prematurity. Rescue treatment with synthetic surfactant therapy has been shown to reduce the incidence of complications of NRDS. Growth and development of infants who received colfosceril palmitate therapy in the study and survived to 1-year adjusted age were equivalent to those of the survivors in the air placebo group. For the cohort of treated infants, colfosceril palmitate reduced the average length of stay at 2 levels of care needed during both the initial hospitalisation (a reduction of 8 days overall and 5 days in intensive care) and all first year hospitalisations (a reduction of 9 days overall and 5 days in intensive care). Total hospital charges for the initial hospitalisation and through 1-year adjusted age for a hypothetical cohort of 100 infants treated with colfosceril palmitate were less than those for a comparable cohort in the air placebo group. The results would, therefore, suggest that rescue therapy with colfosceril palmitate in infants with NRDS and birthweights over 1250g can result in substantial reductions in hospital resource utilisation and charges in addition to the clinical benefits associated with its use.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2002

Determination of vitamin A palmitate in buccal mucosal cells: a pilot study.

We report in our present pilot study on the uptake of retinyl palmitate and its formation to retinol in buccal mucosal cells. Retinoids are able to change metaplastic lesions in several tissues. Prior to any clinical evaluation it is necessary to measure its uptake in target tissues such as the buccal mucosal epithelium. In this pilot study 12 volunteers creamed the inside of their cheeks lightly with a 0.1% retinyl palmitate containing toothpaste for 10 days followed by a wash out phase. On day 0, 3, 7, 10, 17 and 21, buccal mucosal cell samples were taken from volunteers and the uptake of retinol and retinyl palmitate was determined by HPLC analysis. An uptake of vitamin A was demonstrated in all volunteers. Comparing day 0 to day 3 a significant uptake of retinyl palmitate (p<0.05) was detected and comparing day 3 to 17 and 21 a significant decrease (p<0.05) during growth and differentiation of the mucosal epithelium could be seen. The subsequently formed retinol showed an increase but no statistical significance was determined. - The uptake of retinyl palmitate and the formation to retinol led to an enrichment of vitamin A in buccal mucosal cells. In this way metaplastic alterations of the buccal mucosal epithelium might be prevented or reversed by the application of topical retinyl palmitate.

Adult↗
PubMedDate not supplied

Determination of retinyl palmitate (vitamin A) in fortified fluid milk by liquid chromatography: collaborative study.

A liquid chromatographic (LC) method was developed for fast and simple measurement of retinyl palmitate (vitamin A) in fortified milk. Retinyl acetate internal standard was added to a test portion of milk followed by extraction into hexane. The hexane extract was analyzed by LC using a normal-phase silica gel column equilibrated with mobile phase (conditioned hexane-isopropanol, 99.85 + 0.15, v/v) about 1 h before injections. The retinyl palmitate concentration was calculated by using a relative response factor determined with calibration standards. In the collaborative study, 11 laboratories analyzed 13 pairs of fluid milk materials in blind duplicate. Twelve of the materials were composed of skim milk (< 0.5% fat), 1% fat milk, 2% fat milk, and 1% fat chocolate milk. Each material was fortified at 3 concentrations of retinyl palmitate of approximately 581 microg/L (1000 IU/qt), 1163 microg/L (2000 IU/qt), and 2236 microg/L (4000 IU/qt). The 13th material, unfortified skim milk, served as a matrix blank. Repeatability standard deviations (RSDr) without outliers ranged from 1.5 to 5.7% and reproducibility standard deviations (RSDR) without outliers ranged from 5.0 to 22.7%. cis-Isomers co-eluted with the predominant trans-retinyl palmitate isomer and were included in the results reported by all the collaborative laboratories. Endogenous long-chain esters from milk fat were also measured with the retinyl palmitate additive. The Study Director recommends that this method for determination of retinyl palmitate in fluid milk by LC be adopted First Action.

Animals↗
PubMed1991

[Retinol Acetate Reference Standard for Thin-layer Chromatography (Control 901) and Retinol Palmitate Reference Standard for Thin-layer Chromatography (Control 901) of National Institute of Hygienic Sciences].

The raw materials of retinol acetate and retinol palmitate were examined for the preparation of the "Retinol Acetate Reference Standard for Thin-layer Chromatography" and "Retinol Palmitate Reference Standard for Thin-layer Chromatography", respectively. Analytical data obtained were as follows: thin-layer chromatography, no impurities were detected in retinol acetate and one impurities was detected in retinol palmitate; The Rf values of retinol acetate and retinol palmitate were consistent with those of Reference Standards (Control 713), respectively; ultraviolet spectrum, lambda max = 326 approximately 327 nm; relative extinction, within the range reported in JPXI; weight variation of capsules, retinol acetate 224.0 +/- 15.5 mg (RSD 6.9%), retinol palmitate 222.0 +/- 13.8 mg (RSD 6.2%); assay, retinol acetate 57000 I.U./g, retinol palmitate 57000 I.U./g. Based on the above results, these raw materials were authorized to be the Reference Standards of the National Institute of Hygienic Sciences.

Chromatography, Thin Layer↗
PubMed1988

Amniotic fluid cholesteryl palmitate in pregnancies complicated by diabetes mellitus.

Amniotic fluid cholesteryl palmitate, as measured by thin-layer chromatography, appears to be a very sensitive and specific predictor for the risk of respiratory distress syndrome (RDS) in newborns of normal pregnancies. To assess the effect of diabetes mellitus on fetal pulmonary maturation, we measured cholesteryl palmitate concentration, the lung profile, and total phosphatidylcholine in amniotic fluid obtained from 35 well-controlled diabetic and 39 control pregnancies at term. In women with diabetes, the mean (+/- SD) third-trimester glycosylated hemoglobin level was 6.96 +/- 2.3% (normal 6-8%). Mean cholesteryl palmitate concentration in the diabetic population was 79.12 +/- 13.17 micrograms/mL, versus 153.71 +/- 16.77 micrograms/mL in the control group (P less than .001). The mean cholesteryl palmitate concentration was also significantly different for gestational diabetics and class B-R gravidas (112.75 +/- 26.2 versus 54.45 +/- 7.34 micrograms/mL; P less than .005). Cholesteryl palmitate was decreased despite the presence of a mature lecithin/sphingomyelin ratio and, in most cases, phosphatidylglycerol. These data suggest that even in well-controlled diabetic pregnancies, alterations in maternal metabolism may affect either the biosynthesis or degradation of cholesteryl palmitate.

Amniotic Fluid↗
PubMed1998

Apolipoprotein B-48 and retinyl palmitate are not equivalent markers of postprandial intestinal lipoproteins.

This study compared retinyl palmitate and apolipoprotein (apo) B-48 as markers of postprandial triglyceride-rich lipoproteins. Nine non-diabetic men received an oral vitamin A-containing fat load. We measured retinyl palmitate, apoB-48, apoB-100, and triglyceride levels in Sf > 400, Sf 60-400 and Sf 20-60 lipoproteins. The peak retinyl palmitate concentration was delayed compared to the peak apoB-48 concentration in each fraction. The discrepancy between retinyl palmitate and apoB-48 was further investigated in another study of 12 men. In that study, a fat load was given and 5 h later, lipolysis was stimulated in vivo with heparin (60 U/kg, i.v.) and the same parameters were followed. Thirty minutes after heparin, triglyceride levels decreased significantly in the three triglyceride-rich lipoprotein fractions (Sf > 400, Sf 60-400 and Sf 20-60). ApoB-48 levels also fell significantly in the three triglyceride-rich lipoprotein fractions. In contrast, retinyl palmitate concentrations did not change significantly in Sf > 400 and Sf 60-400 fractions and increased significantly in the Sf 20-60 fraction. Our results indicate that retinyl palmitate and apolipoprotein B-48 do not mark the same properties of postprandial intestinal lipoproteins. The metabolic pattern of apolipoprotein B-48 parallels that of triglyceride. One possible explanation for these observations is that the apoB-48-containing triglyceride-rich lipoproteins are metabolically heterogeneous and that older particles, those in circulation for a longer period of time, may be cleared more rapidly than newer ones.

Adult↗
PubMed1982

Incomplete palmitate oxidation. Possible source of human myopathy.

A study of palmitate oxidation in 200 consecutive human muscle biopsy specimens showed 14 patients in whom there was abnormal, incomplete palmitate oxidation when the rate of oxidation of palmitate 14C (ul) was compared with that of palmitate 14C (at carbon 1). Five patients had denervation as a primary diagnosis, and the remaining nine had a primary muscle disease. Of this latter group, six had clinical similarities, including proximal weakness, necrotic fibers on muscle biopsy, and extreme elevations of serum creatine kinase. With one exception, lipid storage was not part of the syndrome. The possibility of incomplete palmitate oxidation due to a defect in beta-oxidation producing a human myopathy is discussed.

Adolescent↗
PubMed1986

Selective use of palmitic acid over stearic acid for synthesis of phosphatidylcholine and phosphatidylglycerol in lung.

The incorporation of [3H]palmitic acid and [14C]stearic acid into phospholipids in rabbit lung tissue was studied. Under equal molar concentrations of palmitate and stearate, palmitate was incorporated to the 1- and 2-positions of phosphatidylcholine (PC) and phosphatidylglycerol (PG) 2-3 times more than stearate. By contrast, palmitate was 30% less than stearate in phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine. These results suggest that preferential utilization of palmitate over stearate, rather than substrate availability, determines the high content of palmitoyl at the 1- and 2-positions of PC and PG in lung.

Animals↗
PubMed1986

Effects of substrate availability on myocardial C-11 palmitate kinetics by positron emission tomography in normal subjects and patients with ventricular dysfunction.

The possibility of demonstrating noninvasively with C-11 palmitate and positron emission tomography (PET) changes in myocardial substrate metabolism in normal and diseased human myocardium in response to altered substrate availability in blood and disease-related abnormalities was examined in five normal volunteers and 16 patients with ventricular dysfunction. C-11 palmitate injection and serial PET imaging were performed after an overnight fast (control period) and again 2 hours later after oral glucose (50 gm). Myocardial C-11 time-activity curves from serial PET images revealed a biexponential clearance pattern. An early rapid phase, defined by relative size and clearance half-time, reflects C-11 palmitate oxidation and the late slow phase tracer deposition in the endogenous lipid pool. During the control period, the tracer fraction entering the early rapid phase averaged 47 +/- 13% (SD) in normal subjects and 45 +/- 12% in patients. Corresponding clearance half-times were 19 +/- 7 and 20 +/- 5 minutes, respectively. Heart rate and blood pressure remained unchanged after glucose, but plasma glucose levels rose by 72.5% in normal subjects and by 98.9% in patients, while free fatty acid levels fell by 72% and 42% (p less than 0.001), respectively. In normal subjects, the tracer fraction in the early rapid phase fell by 43% (p less than 0.005) and the clearance half-time increased by 46% (p less than 0.01). In patients, the response of C-11 palmitate tissue kinetics to glucose was variable. In nine patients, it was similar to that in normal subjects while in the other seven patients a "paradoxic" response occurred. The tracer fraction entering the rapid clearance phase increased after glucose by 30% (p less than 0.05) associated with a 36% (p less than 0.05) decline in clearance half-times. The paradoxic response was unrelated to disease etiology or plasma substrate levels but occurred mostly in left ventricles with more severely depressed function. Thus, PET and C-11 palmitate allow the noninvasive demonstration of the known response of substrate metabolism of the human heart to altered substrate availability. Glucose administration in fasted humans serves as a provocative test of substrate regulation which can be abnormal in myocardial disease and can be demonstrated noninvasively.

Adult↗
PubMed1984

Reconstitution of the lipid-depleted pyruvate oxidase system of Escherichia coli: the palmitic acid effect.

Previous work has shown that the coupling of the soluble Escherichia coli pyruvate oxidase to a lipid-depleted membrane terminal electron transport system requires the addition of ubiquinone and a neutral lipid fraction (C. Cunningham and L. P. Hager (1975) J. Biol. Chem. 250, 7139-7146). The active factor present in the neutral lipid fraction has now been isolated and characterized. NMR, uv, and mass spectroscopic analysis identifies palmitic acid as the active component. A comparison of palmitic acid with other fatty acids of varying chain lengths indicates that most fatty acids having chain lengths in the range C12 to C20 have comparable activity to palmitic acid. Exceptions are stearic and arachidic acid which have greatly reduced activity. Fatty acids of C6 to C10 chain length showed about one third the activity of palmitic acid. Fatty acids having chain lengths of 2 to 5 carbon atoms are essentially inactive. The carboxyl function of the fatty acid is required for activity. Derivatives of fatty acids in which the carboxyl group had been modified to an alcohol, aldehyde, or methyl ester function show greatly diminished activity. Both the cis and trans forms of unsaturated long-chain fatty acids are active. The stimulation of the electron transfer reaction by fatty acids occurs at the ubiquinone level of the electron transport chain. Ubiquinone-30 is rapidly reduced by pyruvate oxidase only in the presence of palmitic acid.

Chemical Phenomena↗
PubMed1988

Regulation of fatty acid oxidation in rat brain mitochondria: inhibition of high rates of palmitate oxidation by ADP.

Regulation of oxidation of [1-14C]palmitate in rat brain mitochondria has been investigated in purified mitochondria of nonsynaptic origin prepared by use of a Ficoll/sucrose density gradient. The mitochondrial preparation contained considerable Mg2+-ATPase activity, but was virtually free of contamination with nonmitochondrial fractions. Palmitate oxidation was inhibited by increasing the concentration of ATP in the assay system to near-physiological levels (2 mM), and the inhibition at 2 or 4 mM ATP was analyzed by comparing it with palmitate oxidation at near-maximal rates with low levels of ATP (0.5 or 1 mM). Inhibition was increased by the addition of ADP or by increasing the concentration of Mg2+ in the assay system, whereas inhibition was decreased by decreasing the concentration of mitochondrial protein or L-carnitine in the assay system. Increasing CoA concentration also had a deinhibitory effect. With 0.5 or 1 mM ATP, however, neither inhibition by added ADP nor protein concentration-dependent inhibition was observed, and the rate of oxidation was saturated with increasing concentrations of Mg2+, L-carnitine, or CoA. These results indicated that ADP was involved in the inhibition of high rates of palmitate oxidation in the presence of sufficient ATP and L-carnitine. The inhibitory effect of increasing the concentration of mitochondrial protein could be explained by the enhanced amounts of ADP present in the preparation; similarly, increased concentrations of Mg2+ would provide higher levels of ADP by stimulating the Mg2+-ATPase reaction. We discuss the possibility that the transport of ADP across the inner membrane of brain mitochondria is coupled to the inhibition of palmitate oxidation.

Adenosine Diphosphate↗
PubMed1995

Uptake and passage of beta-lactoglobulin, palmitic acid and retinol across the Caco-2 monolayer.

Caco-2 cell line grown on collagen coated polycarbonate membranes in bicameral chambers has been used to study the effect of the binding of palmitic acid or retinol on the uptake and passage of iodinated beta-lactoglobulin and albumin across cell monolayers. The percentage of beta-lactoglobulin transported through the monolayer was higher than that of albumin, about 50% and 30% of the total protein after 24 h of incubation, respectively. In all cases, less than 1% of protein was retained intracellularly. No differences were found in the uptake and transport of beta-lactoglobulin or albumin in the presence or absence of ligands. Furthermore, uptake and passage across Caco-2 monolayer of retinol or palmitic acid added either bound to beta-lactoglobulin or to albumin have been compared. The percentage of retinol found in the lower chamber was about 35% of the total retinol after 24 h of incubation for both proteins. However, the amount of retinol associated to cells was higher when it was added bound to beta-lactoglobulin than to albumin, about 26% and 10%, respectively. This fact suggests that the metabolic processing of retinol by Caco-2 cells is the rate-limiting step for retinol transport. The percentage of palmitic acid that crossed the monolayer was about 7%, remaining approx. 90% in the cells for beta-lactoglobulin and albumin. These data support the hypothesis that palmitic acid internalized by Caco-2 cells is mainly destined to serve the structural and energy needs. These results show evidence of retinol and palmitic uptake by Caco-2 cells when beta-lactoglobulin or albumin are the donors, and indicate that the type of binding protein does not affect the transport of both ligands through Caco-2 monolayer.

Biological Transport↗
PubMed1984

Palmitate oxidation in suspended skeletal muscle fibers from the rat.

Palmitate oxidation in rat skeletal muscle was investigated with a suspension of intact isolated cells. M. flexor digitorum brevis was dissociated by a 6 h collagenase treatment to yield single myofibers of which 76% were viable. The contributions of 14CO2 and 14C-labeled acid-soluble intermediates to total oxidation products from palmitate were evaluated. The myofiber suspension exhibited a higher total oxidation rate than the isolated whole muscle, due to improved transport of palmitate to the sarcolemma. Addition of cytoplasmic cofactors L-carnitine, CoASH and ATP did not increase the palmitate oxidation. 14CO2 amounted to about 37% of oxidation products. With [1(-14)C]- and [16(-14)C]palmitate, the oxidation rates were equal. These findings indicate that the cellular integrity was well preserved. The oxidation rates were sharply decreased in fibers with damaged sarcolemmas, and in intact fibers when rotenon and antimycin A were applied. The damaged fibers restored the production of acid-soluble intermediates in the presence of cofactors. The results indicate that suspended skeletal myofibers are an adequate in vitro system for measurements of metabolic activities in the resting muscle.

Animals↗
PubMed1985

Flux of palmitate through the peroxisomal and mitochondrial beta-oxidation systems in isolated rat hepatocytes.

Peroxisomes catalyze the beta-oxidation of fatty acids but their quantitative role in fatty acid catabolism in the intact hepatocyte is not yet clarified. In the present study peroxisomal beta-oxidation of [1-14C]palmitate was quantitated in hepatocytes without the use of metabolic inhibitors. It was assumed that acetyl-CoA formed by peroxisomal beta-oxidation enters the cytosolic pool of acetyl-CoA, whereas that from mitochondrial beta-oxidation enters the mitochondrial pool. The labeling of the two acetyl-CoA pools was assessed by measuring the incorporation of radioactivity into cholesterol (from cytosolic acetyl-CoA) and CO2 (from mitochondrial acetyl-CoA). The system was calibrated with [1-14C]acetate and [1-14C]butyrate because butyrate undergoes beta-oxidation only in mitochondria, whereas acetate forms acetyl-CoA primarily in the cytosol. The labeling ratio, [( 14C]cholesterol X 100)/[( 14C]cholesterol + [14C]CO2), reflects the site of formation of acetyl-CoA. This ratio was 0.51 for butyrate, 1.39 for acetate and 0.79 for palmitate. The difference between palmitate and butyrate was statistically significant (P less than 0.02). This indicates that not all of the palmitate was oxidized in mitochondria. By linear interpolation it was estimated that approximately 32% of the [1-14C]palmitate oxidation began in peroxisomes.

Acetates↗
PubMed1988

Regulation of fetal lung disaturated phosphatidylcholine synthesis by de novo palmitate supply.

Lung surfactant disaturated phosphatidylcholine (PC) is highly dependent on the supply of palmitate as a source of fatty acid. The purpose of this study was to investigate the importance of de novo fatty acid synthesis in the regulation of disaturated PC production during late prenatal lung development. Choline incorporation into disaturated PC and the rate of de novo fatty acid synthesis was determined by the relative incorporation of [14C]choline and 3H2O, respectively, in 20-day-old fetal rat lung explants and in 18-day-old explants which were cultured 2 days. Addition of exogenous palmitate (0.15 mM) increased (26%) choline incorporation into disaturated PC but did not inhibit de novo fatty acid synthesis, as classically seen in other lipogenic tissue. Even in the presence of exogenous palmitate, de novo synthesis accounted for 87% of the acyl groups for disaturated PC. Inhibition of fatty acid synthesis by agaric acid or levo-hydroxycitrate decreased the rate of choline incorporation into disaturated PC. When explants were subjected to both exogenous palmitate and 60% inhibition of de novo synthesis, disaturated PC synthesis was below control values and 75% of disaturated PC acyl moieties were still provided by de novo synthesis. These data show that surfactant disaturated PC synthesis is highly dependent on the supply of palmitate from de novo fatty acid synthesis.

Animals↗
PubMed1989

Regional cerebral incorporation of plasma [14C]palmitate, and cerebral glucose utilization, in water-deprived Long-Evans and Brattleboro rats.

Regional rates of incorporation into brain of intravenously administered [14C]palmitate and regional cerebral metabolic rates for glucose (rCMRglc) were measured in water-provided (WP) and water-deprived (WD) homozygous (DI) and heterozygous (HZ) Brattleboro rats, a mutant strain unable to synthesize vasopressin, and in the parent Long-Evans (LE) strain. Following 15 h or 4 days of water deprivation, rCMRglc was elevated threefold in the pituitary neural lobe of LE-WD and DI-WD as compared with LE-WP rats, and in the paraventricular nucleus of LE-WD, and the supraoptic nucleus of DI-WD rats. However, incorporation of [14C]palmitate into these regions was not specifically altered. The results indicate that water deprivation for up to 4 days increases rCMRglc in some brain regions involved with vasopressin, but does not alter [14C]palmitate incorporation into these regions. Incorporation of plasma [14C]palmitate is independent of unlabeled plasma palmitate at brain regions which have an intact blood-brain barrier, but at nonbarrier regions falls according to saturation kinetics as cold plasma concentration rises, with a mean half-saturation constant (Km) equal to 0.136 mumol.ml-1.

Animals↗
PubMed1984

Synthesis of high purity 11C labeled palmitic acid for measurement of regional myocardial perfusion and metabolism.

Palmitic acid is a major physiological substrate of the myocardium and its role in myocardial metabolism is well understood. 11C labeled palmitic acid may be used with a positron emission tomograph (PET) to obtain high contrast images of transverse sections of the heart. A rapid and reliable method for producing [11C]palmitic acid from [11C]carbon dioxide by the Grignard synthesis is described. All interfering long chain nonradioactive impurities are removed by the purification procedure. As a result, this [11C]palmitic acid may be used as a tracer for pure palmitic acid in the measurement of regional myocardial function.

Animals↗