Maternal dietary protein deficiency decreases amino acid concentrations in fetal plasma and allantoic fluid of pigs

This study was conducted to test the hypothesis that maternal dietary protein deficiency decreases amino acid availability to the fetus, thereby contributing to retarded fetal growth. Primiparous gilts selected genetically for low or high plasma total cholesterol concentrations (low line and high line, respectively) were mated, and then fed 1.8 kg/d of isocaloric diets containing 13% or 0.5% crude protein. At d 40 or 60 of gestation, they were hysterectomized, and maternal and fetal blood samples as well as amniotic and allantoic fluids were obtained for analyses of amino acids, ammonia and urea. Dietary protein restriction decreased (P < 0.05) the following: 1) maternal plasma concentrations of urea at d 40 and 60 of gestation; 2) fetal plasma concentrations of alanine, arginine, branched-chain amino acids (BCAA), glutamine, glycine, lysine, ornithine, proline, taurine, threonine and urea at d 60 of gestation; 3) amniotic and allantoic fluid concentrations of urea at d 40 and 60 of gestation; and 4) allantoic fluid concentrations of alanine, arginine, BCAA, citrulline, cystine, glycine, histidine, methionine, proline, serine, taurine, threonine and tyrosine at d 40 of gestation, in gilts of both genetic lines. At d 60 of gestation, protein deficiency decreased (P < 0.05) allantoic fluid concentrations of arginine, cystine, glycine, taurine and tyrosine in low line gilts and of cystine, glutamine, ornithine, serine, taurine and tyrosine in high line gilts. Low line and high line gilts also differed remarkably in allantoic fluid concentrations of arginine, glutamine, ornithine and ammonia at d 40 and 60 of gestation. Our results suggest the following: 1) protein-deficient gilts maintain maternal plasma concentrations of amino acids by mobilizing maternal protein stores and decreasing oxidation of amino acids during the first half of gestation; 2) protein deficiency may impair placental transport of amino acids from the maternal to the fetal blood; and 3) low line and high line gilts differ in fetal amino acid metabolism. Decreases in concentrations of the essential and nonessential amino acids in the fetus may be a mechanism whereby maternal dietary protein restriction results in fetal growth retardation.     

Taurine, glutamate and GABA modulate the outgrowth from goldfish retinal explants and its concentrations are affected by the crush of the optic nerve

The amino acid taurine plays an important trophic role during development and regeneration of the central nervous system. Other amino acid systems, such as those for glutamate and gamma-aminobutyric acid (GABA), are modified during the same physiological and pathological processes. After crushing the optic nerve, goldfish retinal explants were plated in the absence and in the presence of different amino acids and amino acid receptor agonists. The length and the density of the neurites were measured at 5 days in culture. Taurine increased the length and the density of neurites. Glutamate and glycine increased them at low concentration, but were inhibitors at higher concentration. The combination of N-methyl-D-aspartate (NMDA) and glycine produced a greater inhibitory effect than NMDA alone. NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) added simultaneously with taurine impaired the stimulatory effect of the latter. GABA stimulated the emission of neurites in a concentration dependent manner. Hypotaurine also elevated the length of neurites, but cysteinsesulfinic acid did not produce a significant effect. The concentrations of taurine, glutamate and GABA were determined by HPLC with fluorescent detection in the retina of goldfish at various days post-crushing the optic nerve. The levels of taurine were significantly increased at 48h after the crush, and were elevated up to 20 days. Glutamate level decreased after the lesion of the optic nerve and was still low at 20 days. GABA concentration was not significantly different from the control. The interaction of these amino acids during the regenerative period, especially the balance between taurine and glutamate, may be a determinant in restoring vision after the crush.     

Changes of renal taurine transport after treatment with triiodothyronine or dexamethasone in amino acid loaded rats

In adult female anaesthetized rats, the influence of triiodothyronine or dexamethasone on renal amino acid (AA) handling was investigated in taurine (45 mg/100 g b.wt.) loaded animals. Bolus injections of taurine were followed by temporary increase in fractional excretion (FE(AA)) of taurine as well of the endogenous amino acids which were not administered. Under taurine load conditions, triiodothyronine treatment (20 microg/100 g b.wt. for 3 days, i.p. once daily) was followed by a slight stimulation of the renal taurine reabsorption: the increase in FE(taurine) after taurine load was lower than in untreated rats. Dexamethasone (60 microg/100 g b.wt. for 3 days, i.p. once daily) was without significant effect on FE(taurine) in taurine loaded rats. In non taurine loaded rats there was no hormone influence at all. Similarities and differences between the effects of bolus injections of taurine, glutamine, and leucine on the FE(AA) of these three amino acids were compared in detail to further clarify the reason for the increased amino acid reabsorption capacity after pretreatment with triiodothyronine or dexamethasone.     

Protein kinase inhibitors attenuate cardiac swelling-induced amino acid release in the rat

Rat Langendorff heart preparations have been used to study the efflux of cardiac amino acids into coronary artery perfusates during brief (5-min) periods of exposure to hyposmotic stress (70 mM NaCl). Coronary flow rates, heart rates and intra-aortic pressures were recorded. Amino acid levels were measured by high-performance liquid chromatography. Hyposmotic stress caused marked percentage increases in taurine, glutamate and aspartate levels in the coronary perfusate, with smaller increases in phosphoethanolamine, glycine and alanine and non-significant increases in serine and glutamine. Amino acid levels declined during reperfusion with isosmotic Krebs-Henseleit bicarbonate buffer. Inhibition of protein kinase C with chelerythrine chloride (5 microM) depressed the osmotically-induced release of aspartate, glutamate, taurine and glycine. The protein tyrosine kinase inhibitor, genistein, reduced the anisosmotic efflux of aspartate, glutamate, taurine and phosphoethanolamine. Lavendustin A, another inhibitor of tyrosine kinase, depressed the osmotically evoked release of aspartate, glutamate and taurine. These studies demonstrate the involvement of protein kinase C and tyrosine kinases in the efflux of amino acids from the osmotically challenged rat heart and imply that these enzymes are involved in the mechanisms responsible for volume regulation by cardiac cells.     

Taurine: protective properties against ethanol-induced hepatic steatosis and lipid peroxidation during chronic ethanol consumption in rats

Alcohol was administered chronically to female Sprague Dawley rats in a nutritionally adequate totally liquid diet for 28 days. This resulted in hepatic steatosis and lipid peroxidation. Taurine, when co-administered with alcohol, reduced the hepatic steatosis and completely prevented lipid peroxidation. The protective properties of taurine in preventing fatty liver were also demonstrated histologically. Although alcohol was found not to affect the urinary excretion of taurine (a non-invasive marker of liver damage), levels of serum and liver taurine were markedly raised in animals receiving alcohol + taurine compared to animals given taurine alone. The ethanol-inducible form of cytochrome P-450 (CYP2E1) was significantly induced by alcohol; the activity was significantly lower than controls and barely detectable in animals fed the liquid alcohol diet containing taurine. In addition, alcohol significantly increased homocysteine excretion into urine throughout the 28 day period of ethanol administration; however, taurine did not prevent this increase. There was evidence of slight cholestasis in animals treated with alcohol and alcohol + taurine, as indicated by raised serum bile acids and alkaline phosphatase (ALP). The protective effects of taurine were attributed to the potential of bile acids, especially taurine conjugated bile acids (taurocholic acid) to inhibit the activity of some microsomal enzymes (CYP2E1). These in vivo findings demonstrate for the first time that hepatic steatosis and lipid peroxidation, occurring as a result of chronic alcohol consumption, can be ameliorated by administration of taurine to rats.     

Comparison of the actions of glycine and related amino acids on isolated third order neurons from the tiger salamander retina

Whole cell voltage and current clamp recordings were obtained from third order neurons isolated from the salamander retina. Using cross desensitization, the structure-function relationship of short chain amino acids on the glycine receptor were examined. L-Serine, L-alanine, beta-alanine and taurine all cross desensitized with glycine, but did not show significant cross desensitization with GABA. This indicates that these amino acids act at the glycine receptor. The order of potency was glycine > beta-alanine > taurine > L-alanine > L-serine. TAG, a reputed selective taurine antagonist, was equally effective in blocking taurine and glycine currents. There is no evidence for distinct receptors for taurine. Amino acids with larger moieties at the alpha carbon, such as threonine and valine, produced inactive ligands. Placing a methyl group on the amine of glycine or esterification of the carboxyl group also greatly reduced activity. Based on these modifications of the glycine molecule, it appears that selectivity at the glycine receptor results in part from steric restrictions at all three sites in the glycine chain. The steric interference is most critical at the carboxyl and amino ends, and less limiting at the alpha carbon. Doses of L-serine that had only slight effects in voltage clamp experiments, nevertheless produced large effects in current clamp experiments. This indicates that several endogenous amino acids can have significant effects on membrane voltage, even when their shunting activity may be small. High concentrations of agonists produced desensitization in the voltage clamp records, but there was little evidence of desensitization in the current clamp experiments. These results indicate that several endogenous amino acids can activate the glycine receptor, but there is no evidence for a discrete receptor for taurine, beta-alanine, L-alanine or L-serine. Since all these endogenous amino acids have similar amino and acid terminals, reduction in potency results from steric interference around the alpha carbon. This graded potency may have functional significance in mediating inhibition.     

Attitudes about cancer pain: a survey of 727 health care professionals in West Virginia

Different catabolic conditions have their special characteristics of intracellular biochemical changes. The objective of the presented work is to assess the concentration of free amino acids in muscles of patients with colorectal carcinoma. In a group of 17 patients the free amino acid level was assessed in tissues and plasma. Material was collected on operation by biopsy of the rectus abdominis muscle, the concentration of different amino acids was assessed by the HPLCV method with fluorescent detection. For statistical evaluation the T-test was used. From the results ensues that in patients with colorectal cancer in plasma statistically significantly lower taurine, glutamine, valine, tyrosine levels were found, intracellularly significantly reduced levels of taurine, glutamic acid, methionine and ornithine were recorded. Significantly elevated intracellular levels of valine, isoleucine, leucine, tyrosine and phenylalanine were found. Assessment of the tissue aminoacidogram is the first step when attempting to influence the intracellular amino acid concentration by defined dietetic preparations.     

Longitudinal changes of brain amino acid content occurring before, during and after epileptic activity

In cats affected with cortical epileptogenic foci induced by penicillin application to and cobalt implantation into the pericruciate area, the brain amino acids contents were determined in the focus as well as in extrafocal areas. In different groups of animals, brain removal for biochemical determinations was performed at different times before, during and after epilepsy and the values compared to controls. The only amino acid to show a significant change before appearance of spikes in both types of epilepsy was taurine, which decreased. Cobalt epilepsy was accompanied by changes in a larger number of amino acids than penicillin epilepsy: in the former the brain content of taurine, GABA, aspartate, glutamate, serine, threonine, glycine and alanine was altered. The changes were proportional to the severity of epilepsy and more prominent in the focus area. After disappearance of spikes the levels of most amino acids returned to normal except for some amino acids, previously unaffected by penicillin epilepsy, which were decreased. It is proposed that the decrease in brain taurine, occurring before the appearance of penicillin and cobalt epilepsy, could increase the excitability of a certain neuronal population and thus, by potentiating the effects on neurons of penicillin and cobalt, contribute to the initiation of epilepsy.     

Spinal amino acid release and precipitated withdrawal in rats chronically infused with spinal morphine

Glutamate receptors are implicated in the genesis of opioid tolerance and dependence. Factors governing release of amino acids in systems chronically exposed to opiates, however, remain undefined. Using rats, each prepared with a spinal loop dialysis catheter and with a chronic lumbar intrathecal infusion catheter connected to a subcutaneous minipump, the release of amino acids before and during antagonist-precipitated withdrawal in unanesthetized rats was examined. Spinal infusion of morphine (20 nmol/micro l/hr) for 4 d had little effect on resting release of amino acids. In morphine-infused, but not saline-infused, rats naloxone (2 mg/kg, i.p.) evoked an immediate increase in the release of L-glutamate (299 +/- 143%) and taurine (306 +/- 113%) but not other amino acids. The magnitude and time course of the release of these amino acids significantly correlated with behavioral indices of withdrawal intensity. Acute intrathecal pretreatment immediately before naloxone with clonidine (20 microg; alpha2 agonist), MK-801 (3 microg; noncompetitive NMDA antagonist), or aminophosphonopentanoic acid (AP-5; 3 microg; competitive NMDA antagonist) suppressed naloxone-induced increases in spinal L-glutamate and taurine release and behavioral signs of withdrawal in spinal morphine-infused rats. Results point to a correlated increase in spinal L-glutamate release, which contributes to genesis of the opioid withdrawal syndrome. Agents such as clonidine that suppress opioid withdrawal may owe their action to an inhibition of excitatory amino acid release. The effects of MK-801 and AP-5 suggest a glutamate-evoked glutamate release.     

Action of amino acids and convulsants on cerebellar spontaneous action potentials in vitro: effects of deprivation of C1-, K+ of Na+

(1) The inhibition of spontaneous action potentials in guinea pig cerebellar cortex slices by GABA, glycine, taurine and beta-alanine is maintained when C1- in the superfusion medium is almost completely replaced by NO3- or I-('permeant' anion), but the inhibition decreases in magnitude with repeated application of the amino acid. Replacement of C1- by sulfate or isethionate ('impermeant' anion) causes a conversion of inhibition by these amino acids to excitation. The initial excitation which is sometimes seen with these inhibitory amino acids in high C1- media is abolished when C1- is replaced by either permeant or impermeant anions. (2) Reduction of K+ in the medium causes an increase of inhibition by the inhibitory amino acids in the presence of high C1- and reduction of excitation when C1- is replaced by impermeant anion. (3) Excitation by GABA in impermeant anion (low C1-) media is unaffected by reduction of Na+ in the media by 50% but excitations by glycine, taurine, beta-alanine and L-glutamate are greatly reduced. (4). Excitation by GABA in impermeant anion (low C1-) media is abolished by picrotoxin and bicuculline which both suppress inhibition by GABA in a high C1- medium. Strychnine suppresses the effects of glycine, taurine and beta-alanine in either a low or high C1- medium. Bicuculline blocks the inhibitory effect of these three amino acids in a high C1- medium but does not affect their excitatory effects in a low C1- medium. (5) These results are consistent with the hypothesis that the inhibitory amino acids, GABA, glycine, taurine and beta-alanine, cause inhibition via increase of C1- (and perhaps K+) permeability and that glycine, taurine and beta-alanine also interact with strychnine-sensitive receptors mediating (perhaps indirectly) increased permeability to Na+ and, therefore, excitation in low C1- media.     

Comparison of the development of the fatty acid content and composition of the brain of a precocial species (guinea pig) and a non-precocial species (rat)

The fatty acid compositions of the brains of a precocial (guinea pig) and a non-precocial (rat) species have been studied as a function of development. In the rat brain the total fatty acid content expressed as mg g wet wt.-1 increased more than fourfold during the period from 5 days after birth to adulthood. However, the percentage composition of this total fatty acid content when expressed per individual fatty acid remained fairly constant, with the exception of nervonic acid (C24:1) which also increased fourfold on a percentage basis. In the guinea pig brain, however, at birth the total fatty acid content, expressed as mg g wet wt-1, is the same as that of the adult, the concentration doubling during the period from 25 days before birth until birth. Again, if the fatty acid content is analysed and expressed on a percentage basis, the relative concentrations of the individual fatty acids remain fairly constant over the period from 25 days before birth until adulthood, with the exception of nervonic (C24:1) acid which increases about fivefold from 25 days before birth to birth and only marginally (20%) from birth to adulthood. These results are discussed in relationship to the onset of neurological competence in the two species. It is concluded that the increase in fatty acid content (both total and individually) of the brains of these species as a function of the foetal and neonatal development follows a pattern which is similar to the pattern of development of certain key enzymes of energy metabolism and of neurological competence.     

Age-specific distribution of plasma amino acid concentrations in a healthy pediatric population

Reference values were determined for 23 plasma free amino acids from measurements done in 148 healthy children ranging from 0 to 18 years of age. Amino acid analysis was performed by ion-exchange chromatography. We propose a graphic form of presenting the age-specific distribution of plasma amino acid concentrations where the 10th, 50th, and 90th quantiles are illustrated. Although each amino acid possesses its own pattern of distribution, we can identify five different profiles. Nine amino acids (alanine, arginine, asparagine, methionine, ornithine, phenylalanine, proline, threonine, and tyrosine) demonstrate a decrease in their concentrations during the first year of life; their concentrations then tend to increase throughout childhood and adolescence. Nine others (cystine, glutamine, glycine, histidine, isoleucine, leucine, lysine, tryptophan, and valine) show a steady increase throughout infancy, childhood, and adolescence. Five amino acids (aspartic acid, citrulline, glutamic acid, serine, and taurine) do not follow these two common profiles. For the first time, quantile curves are produced to illustrate the age-dependent variation of amino acid concentrations from infancy to adulthood. This alternative way of presenting amino acid concentrations may facilitate the follow-up of patients with inborn errors of amino acid metabolism.     

Metabolic response to standardised exercise test in standardbred trotters with red cell hypervolaemia

Plasma concentrations of lactate, amino acids, ammonia and products of purine catabolism were studied before, during and after a standardised incremental exercise test in 29 Standardbred trotters admitted to the clinic for exercise tolerance testing. According to their red cell volume the horses were divided into red cell normovolaemic and red cell hypervolaemic (polycythaemic) groups. The exercise-response curve for taurine differed significantly in the two groups, whereas all the other amino acids behaved similarly. The [branched-chain amino acid]/[alanine] ratio, a proposed indicator for the use of amino acids in gluconeogenesis, was at rest significantly higher in the polycythaemic horses. Post-exercise concentrations of ammonia and allantoin, both end products of ATP breakdown, were lower in the polycythaemic horses. No differences were observed in the VLA4 and V200 markers for lactate and heart rate responses to incremental exercise, the oxidative capacity of the gluteus medius muscle, the enzyme activities or the post-exercise concentration of lactate, uric acid and hypoxanthine. It is concluded that horses with red cell hypervolaemia behave in a submaximal standardised exercise test on a treadmill in the same way as do red cell normovolaemic horses. The results suggest that the rate of amino acid utilisation in gluconeogenesis and the ability of amino acids to produce energy aerobically may be elevated in polycythaemic horses.     

Effects of repeated cerebral ischemia on extracellular amino acid concentrations measured with intracerebral microdialysis in the gerbil hippocampus

BACKGROUND AND PURPOSE: To clarify the role of elevated extracellular amino acid concentrations during ischemia on the cumulative neuronal damage after repeated cerebral ischemic insults, using a microdialysis technique we measured concentrations of the amino acids glutamate, glutamine, glycine, taurine, and gamma-aminobutyric acid in the gerbil hippocampus over three 2-minute forebrain ischemic insults induced at 1-hour intervals. METHODS: Under light anesthesia, the bilateral common carotid arteries were occluded with aneurysm clips at 1-hour intervals. Samples were collected by microdialysis at 10-minute intervals, and the amino acid concentrations were determined using a high-performance liquid chromatography system. RESULTS: During and immediately after the first ischemic insult, concentrations of glutamate, glycine, and taurine, but not glutamine, increased significantly. Glutamate and taurine concentrations rose again during the second and third ischemic insults, but the increases were smaller than those during the first insult. By contrast, glutamine concentrations increased slightly but significantly during the second and third ischemic insults. The extracellular concentration of gamma-aminobutyric acid before the ischemic insults was below the level of detectability but increased markedly during each ischemic insult, with similar declines in the amounts released during later insults. Concentrations of all amino acids returned to baseline after 10 minutes of reperfusion and remained at baseline until the subsequent ischemic insult was induced. CONCLUSIONS: It is well established that glutamate released during ischemia plays a crucial role in ischemia-induced neuronal death. However, the present results indicate that cumulative neuronal damage following sublethal ischemic insults is not caused by an exaggerated release of excitatory amino acids during subsequent ischemic insults but strongly suggest that increased intracellular reactions leading to cell death play a major role.     

Mechanisms for oliguria in acute renal failure

Equations previously developed to describe the enterohepatic circulation of the major biliary bile acids in man (Gastroenterology 67:887, 1974) were modified in order to predict the effect on biliary bile acid composition and pattern of amino acid conjugation after prototypic perturbations of the enterohepatic circulation in man. For the steroid moiety, the effects of bile acid feeding, increased recycling frequency, decreased intestinal conservation, and increased dehydroxylation were simulated. For the glycine or taurine moiety, the effect of increased deconjugation or preferential loss of one of the amino acid moieties was simulated. For the steroid moiety, the steady state biliary bile acid composition reflects the balance between input and conservation for each bile acid. Similarly, the distribution of bile acids between glycine and taurine conjugates reflects the balance between conjugation and conservation for each amino acid moiety. Because these values may vary widely and independently, analysis of biliary bile acid composition in terms of the steroid moiety or the glycine-taurine ratio per se cannot be used to infer the relative rates of input or conjugation.     

The clinical significance of type 1 fiber predominance

Having recently demonstrated that taurine supplementation prevents total parenteral nutrition (TPN)-induced cholestasis, we chose to use this model to examine plasma membrane composition in relation to bile formation. Male guinea pigs received daily a mixture of glucose and of the amino acid solution Travasol with or without added taurine (1.2 mM). After 3 days, bile was collected and liver plasma membrane fractions enriched in sinusoidal lateral membrane and bile canalicular membrane domains were isolated. In animals receiving TPN alone, bile flow and biliary secretory rate of bile acid and bicarbonate decreased significantly compared with controls. Although membrane ATPases (Na+K+ and Mg+) were unchanged, TPN induced an increase in the lipid to protein ratio and a decrease of polyunsaturated fatty acids, in conjunction with a higher content of diene conjugates in sinusoidal lateral membrane fractions. Taurine corrected these changes and, in addition, reduced significantly the cholesterol to phospholipid ratio in both membrane fractions. The data show that changes in liver cell membranes occur in TPN-induced cholestasis and suggest that free radical injury may play a role. As taurine prevented cholestasis as well as membrane changes, it is suggested that taurine should be added to amino acid solutions used for parenteral nutrition.     

The role of the locus coeruleus and N-methyl-D-aspartic acid (NMDA) and AMPA receptors in opiate withdrawal

The turnover rates of plasma lactate, normalized for O2 consumption rate, are higher in the fetus than in the adult. This occurs despite very low rates of fetal gluconeogenesis which preclude the recycling of lactate carbon into glucose. In an effort to establish the main routes of disposal of fetal plasma lactate, 12 midgestation ovine fetuses (age 74 +/- 1 days) were infused intravenously at constant rate with L-[U-14C]lactate for a 4-hour period. At the end of the infusion, the amounts of 14C retained by the fetus and by the placenta, and the distribution of the retained 14C in free and protein-bound amino acids and in lipids were measured. Of the total 14C infused, 17.0 +/- 1.4% was recovered in the placenta, 4.0 +/- 0.3% in the fetal liver, and 15.0 +/- 0.8% in the extrahepatic fetal tissues. Of the retained radioactive carbon, 45-57% was recovered in the free and protein-bound amino acid fractions and 11-17% in the lipid fractions. Approximately 90% of the 14C in the free amino acid fractions was present as glutamate/glutamine, serine, glycine, and alanine carbon. In conjunction with data on fetal CO2 production from lactate carbon, these results demonstrate that the main routes of fetal lactate disposal are oxidation and synthesis of nonessential amino acids and lipids.     

Effect of ischaemia and reperfusion on the intracellular concentration of taurine and glutamine in the hearts of patients undergoing coronary artery surgery

Taurine and glutamine are the most abundant intracellular free amino acids in mammalian hearts where changes in their intracellular concentrations are likely to influence a number of cellular activities. In this study we investigated the effects of ischaemia and reperfusion on the intracellular concentrations of taurine and glutamine in the hearts of patients undergoing coronary artery bypass surgery using cold crystalloid or cold blood cardioplegic solutions. Ischaemic arrest (30 min), using cold crystalloid cardioplegic solution (n = 19), decreased the intracellular concentrations (micromol/g wet weight) of taurine (from 9.8 +/- 0.8 to 7.7 +/- 0.7, P < 0.05) and glutamine (8.7 +/- 0.5 to 7.2 +/- 0.6). After 20 min of normothermic reperfusion the fall in taurine and glutamine was maintained (7.5 +/- 0.5 and 7.4 +/- 0.7 for taurine and glutamine respectively). Myocardial ischaemic arrest with cold blood cardioplegic solution (n = 16) did not cause a significant fall in tissue taurine or glutamine. However, on reperfusion there was a marked fall in the intracellular concentrations of taurine (9.4 +/- 0.5 to 6.5 +/- 0.7) and glutamine (8.0 +/- 0.7 to 5.8 +/- 0.4). The fall in amino acids was associated with a fall in ATP and a rise in tissue lactate. This work demonstrates that irrespective of the cardioplegic solution used to arrest the heart, there is a marked fall in tissue taurine and glutamine which may influence the extent of recovery following surgery. The fall in taurine is largely due to efflux whereas changes in glutamine are due to both transport and metabolism. Ischaemia, hypothermia and changes in the transmembrane concentration gradients are the likely factors responsible for the changes in tissue amino acids.     

The hepato-renal syndrome: renal amino acid transport in bile duct ligated rats (DL)--influence of treatment with triiodothyronine or dexamethasone on renal amino acid handling in amino acid loaded rats

The influence of triiodothyronine or dexamethasone on renal amino acid handling was investigated in anaesthetized, bile duct-ligated (DL) adult female rats. 3 days after DL, glomerular filtration rate (GFR) was unchanged whereas urine flow was decreased. Plasma concentrations of 5 out of 16 amino acids were significantly enhanced after DL. On the other hand, the fractional excretion (FE) of 11 out of 16 amino acids was significantly reduced as a sign of improved reabsorption capacity. Bolus injections of leucine (20 mg/100 g b.wt.), glutamine (45 mg/100 g b.wt.), or taurine (45 mg/100 g b.wt.) were followed by a temporary increase in the FE of the administered amino acids as well of the endogenous amino acids which were not administered. This phenomenon was more pronounced in DL than in control rats. Under load conditions, dexamethasone (60 microg/100 g b.wt.) or triiodothyronine (20 microg/100 g b.wt.) treatment for 3 days, i.p. once daily, was followed by a stimulation of renal amino acid reabsorption in DL rats. The increase in fractional amino acid excretion after amino acid load was significantly lower than in untreated rats. This effect was also more pronounced in DL rats.     

Isolation and characterization of a 230 kDa protein (p230) specifically expressed in fetal brains: its involvement in neurite outgrowth from rat cerebral cortex neurons grown on monolayer of astrocytes

By screening with monoclonal antibodies (mAbs) raised against growth cone membrane fraction from fetal porcine brains, we have identified a 230 kDa antigen, termed p230. Western blot analysis of extracts from various tissues demonstrated that p230 is specifically expressed in brains, in which its expression is temporally restricted; it was especially prominent in the embryonic and the early postnatal stage, and decreased to subdetectable levels in the adult brain. Further characterization of p230 revealed that it is a peripherally-membrane associated, cell surface protein produced by astrocytes. Neurite outgrowth of E18 rat cerebral cortex neurons cultured on a monolayer of astrocytes was significantly reduced in the presence of anti-p230 polyclonal antibody. Partial amino acid sequences of p230 purified from fetal porcine brains were highly homologous to an extracellular matrix protein, tenascin-C. These lines of evidence suggest that p230, a tenascin-C-like molecule present in fetal porcine brains, plays important roles during early brain development, particularly in growth cone guidance.