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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to compare the effects of drinking two carbohydrate (CHO) electrolyte solutions and water on marathon running performance. Seven endurance-trained runners completed three 42.2-km treadmill time-trials which were randomly assigned and 4 weeks apart. On each occasion the subjects ingested 3 ml.Kg-1 body weight of either water (W), a 6.9% CHO solution (O) or a 5.5% CHO solution (L) immediately prior to the start of the run and 2 ml.kg-1 body weight every 5 km thereafter. The total volume of fluid ingested [mean (SEM)] was 1112 (42), 1116 (44) and 1100 (44) ml, respectively. Running times for W, O and L trials were 193.9 (5.0), 192.4 (3.3) and 190.0 (3.9) min, respectively. Performance time for the L trial was faster (P < 0.05) compared with that of the W trial. Running speed was maintained in the L trial, whereas it decreased after 10 km (P < 0.05) in the W and after 25 km (P < 0.05) in the O trial. Blood glucose and lactate, and hormonal responses to fluid ingestion were similar in all three trials. Higher plasma free fatty acid and glycerol concentrations were observed at the end of the W trial compared with those obtained after the O and L trials, respectively (P < 0.05). Plasma ammonia concentration was higher (P < 0.01) at the end of the L trial compared with the W trial. Plasma creatine kinase concentration was higher (P < 0.05) 24 h after the completion of the L trial than after the W trial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of carbohydrate-electrolyte drinks on marathon running performance. 776 38

This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.
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PMID:Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis. 782 75

Hyperammonemia is thought to be important in the pathogenesis of hepatic encephalopathy. However, the mechanism leading to ammonia toxicity is still not known. Since the metabolism of the most important excitatory neurotransmitter, glutamate, is closely linked to that of ammonia, it has been postulated that hyperammonemia lowers the availability of the neurotransmitter glutamate. To study this hypothesis, we used brain dialysis to measure glutamate levels in extracellular cerebral fluid from rabbits with acute ischemic liver failure or acute hyperammonemia. The basal glutamate concentration was found to be increased during both acute liver failure (start of experiments 4.9 +/- 1.7 mumol/l; end of experiments 9.5 +/- 2.1 mumol/l, n = 6, difference p < 0.05) and acute hyperammonemia (start of experiments 4.4 +/- 1.2 mumol/l; end of experiments 7.3 +/- 1.8 mumol/l, n = 7, difference p > 0.05) (mean +/- SEM). Both the veratridine- and the potassium-evoked glutamate release were increased during acute liver failure but appeared normal during hyperammonemia. We conclude that during acute liver failure and acute hyperammonemia in the rabbit there is no decreased glutamate availability in the extracellular space of the cortical brain; on the contrary, we found evidence for increased extracellular glutamate concentrations in the cortical brain, which were more pronounced in acute liver failure. Experimental hepatic encephalopathy is thus not due to cerebral glutamate deficiency.
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PMID:Extracellular brain glutamate during acute liver failure and during acute hyperammonemia simulating acute liver failure: an experimental study based on in vivo brain dialysis. 791 Nov 35

The aim of this study was to investigate whether, when muscle glycogen is reduced, a pre-exercise infusion of branched-chain amino acids (BCAA) modifies exercise performance or the metabolic and respiratory responses to incremental exercise. Six moderately trained volunteers took part in the following protocol on two occasions. On day 1, at 9 a.m. in the postabsorptive state, they performed a graded incremental exercise (increases of 35 W every 4 min) to exhaustion (Ex-1). A meal of 1,000 kcal (4,200 kJ; 60% protein, 40% fat) was consumed at 12 p.m. No food was then allowed until the end of the experiment (20-21 h later). A 90-min period of exercise at alternating high and moderate intensities, designed to deplete muscle glycogen, was performed between 6 p.m. and 7.30 p.m. The morning after (day 2), the subjects randomly received either a mixed solution of BCAA (260 mg x kg-1 x h-1 for 70 min), or saline. They then repeated the graded incremental exercise to exhaustion (Ex-2). Metabolic and respiratory measurements suggested a muscle glycogen-depleted state had been achieved. No significant differences were observed in total work performed, maximal oxygen uptake or plasma ammonia, alanine, and blood pyruvate concentrations in the two treatments. After BCAA infusion, higher blood lactate concentrations were observed at maximal power output in comparison with those during saline [BCAA 4.97 (SEM 0.41) mmol x l-1, Saline 3.88 (SEM 0.47) mmol x l-1, P < 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of infusing branched-chain amino acid during incremental exercise with reduced muscle glycogen content. 795 52

The effect of ethyl alcohol on upper airway reflex sensitivity (UARS) has not been previously investigated in humans. Using a technique that we have previously described, intermittent breaths of low concentrations of ammonia vapour were used to measure the effect of ethyl alcohol 0.55-0.66 g/kg on UARS in ten healthy male volunteers. The depression of upper airway reflexes that occurred following ingestion of ethyl alcohol was maximum at 60 min and returned to baseline by 150 min. This dose of ethyl alcohol was insufficient to produce statistically significant depression of UARS. The blood alcohol levels achieved showed a wide range with a mean of 78.9 mg/100 ml (SEM 10.3). Individual subjects who had blood alcohol levels in excess of 100 mg/100 ml displayed much greater depression of UARS. In conclusion, 0.55-0.66 g/kg ethyl alcohol given to healthy male volunteers does not produce significant depression of UARS as measured using an ammonia stimulus technique.
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PMID:The effect of ethyl alcohol on the sensitivity of upper airway reflexes. 798 80

In experimental hepatic encephalopathy and hyperammonemia, extracellular levels of glutamate are increased in hippocampus and cerebral cortex. It has been suggested that overstimulation of glutamate receptors causes a pathological entry of calcium into neurons via receptor-operated (NMDA- and AMPA-type) or voltage-dependent calcium channels leading to calcium overload and cell death. Neurodegeneration as a result of exposure to excitotoxins, including glutamate, can be localized and quantified using 45CaCl2 autoradiography. This approach was used to study cerebral calcium accumulation in rabbits with acute liver failure and acute hyperammonemia. Acute liver failure was induced in 6 rabbits, acute hyperammonemia in 4 rabbits; 4 control rabbits received sodium-potassium-acetate. At the start of the experiment 500 microCi 45CaCl2 was given intravenously. After development of severe encephalopathy, the animals were killed by decapitation. All rabbits with acute liver failure or acute hyperammonemia developed severe encephalopathy, after 13.2 +/- 1.7 and 19.3 +/- 0.5 hours respectively (mean +/- SEM). Plasma ammonia levels were 425 +/- 46 and 883 +/- 21 mumol/l, respectively (p < 0.05). Control rabbits maintained normal plasma ammonia levels (13 +/- 5 mumol/l), demonstrated normal behaviour throughout the study and were sacrificed after 16 hours. 45Ca(2+)-autoradiograms of 40 microns brain sections were analyzed semiquantitatively using relative optical density and computerized image analysis. As compared to background levels 45Ca was not increased in hippocampus or any other brain area of rabbits with severe encephalopathy from acute liver failure or acute hyperammonemia. This suggests that, despite increased extracellular brain glutamate levels in these conditions, glutamate neurotoxicity was not important for the development of encephalopathy in these rabbits.
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PMID:45CaCl2 autoradiography in brain from rabbits with encephalopathy from acute liver failure or acute hyperammonemia. 807 63

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 x 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth and reproductive performance, during exposure to ammonia, of gilts afflicted with pneumonia and atrophic rhinitis. 811 50

This study was designed to quantify the effect of dietary manganese deficiency on rat hepatic Mn concentration and arginase activity. Weanling male Sprague-Dawley rats were randomly assigned to two groups of nine rats each and fed L-amino acid diets with 0 or 48 micrograms Mn/g diet for 21 d. After 21 d, hepatic Mn concentration (mumol/g liver dry wt, mean +/- SEM) was 0.130 +/- 0.005 for the control group but was lower (P < 0.01) in the Mn-deficient group (0.040 +/- 0.003). There were no differences in the hepatic concentrations of any other measured mineral. Hepatic arginase activity [mmol ornithine/(g hepatic protein.min)] was 1.55 +/- 0.22 in the control group and was lower (P < 0.01) in the Mn-deficient group (1.12 +/- 0.26). Plasma ammonia concentration was 301 +/- 6 mumol/L in the control group and was higher (P < 0.01) in the Mn-deficient group (480 +/- 8 mumol/L). In contrast, plasma urea concentration was higher (P < 0.01) in the control group (350 +/- 10 mumol/L) than in the Mn-deficient group (267 +/- 7 mumol/L). There were no differences in plasma concentrations of arginine or other amino acids between the control and the Mn-deficient groups. Our results demonstrate for the first time that dietary Mn deficiency results in altered plasma concentrations of ammonia and urea in association with decreased hepatic Mn concentration and arginase activity in young growing rats.
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PMID:Dietary manganese deficiency decreases rat hepatic arginase activity. 812 Jun 52

Metabolic activity of a gel-entrapment, hollow fiber, bioartificial liver was evaluated in vitro and during extracorporeal hemoperfusion in an anhepatic rabbit model. The bioartificial liver contained either 100 million rat hepatocytes (n = 12), fibroblasts (n = 3), or no cells (n = 7) during hemoperfusion of anhepatic rabbits. Eight other anhepatic rabbits were studied without hemoperfusion as anhepatic controls, and three sham rabbits served as normal controls. Albumin production rates (mean +/- SEM) were similar during in vitro (17.0 +/- 2.8 micrograms/h) and extracorporeal (18.0 +/- 4.0 micrograms/h) application of the hepatocyte bioartificial liver. Exogenous glucose requirements were reduced (p < 0.01) and euglycemia was prolonged (p < 0.001) in anhepatic rabbits treated with the hepatocyte bioartificial liver. The maximum rate of glucose production by the hepatocyte bioartificial liver ranged from 50-80 micrograms/h. Plasma concentrations of aromatic amino acids, proline, alanine, and ammonia were normalized in anhepatic rabbits during hepatocyte hemoperfusion. Gel-entrapped hepatocytes in the bioartifical liver performed sulfation and glucuronidation of 4-methylumbelliferone. P450 activity was demonstrated during both in vitro and extracorporeal application of the BAL device by the formation of 3-hydroxy-lidocaine, the major metabolite of lidocaine biotransformation by gel-entrapped rat hepatocytes. In summary, a gel-entrapment, bioartificial liver performed multiple hepatocyte-specific functions without adverse side effects during extracorporeal application in an anhepatic, small animal model. With its potential for short term support of acute liver failure, scale-up of the current bioartificial liver device is indicated for further investigations in large animal, preclinical trials.
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PMID:Extracorporeal application of a gel-entrapment, bioartificial liver: demonstration of drug metabolism and other biochemical functions. 816 29

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26


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