bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased hepatic amino nitrogen conversion after elective cholecystectomy in man
Authors: Heindorff Hans , Vilstrup Hendrik , Bucher Ditlev , Billesbølle Per , Thygesen Vibeke 
Published: August 2015

1. The effect of elective, uncomplicated cholecystectomy on plasma clearances of amino acids and on amino acid-stimulated urea synthesis was investigated in 10 patients, pre-operatively and on the first post-operative day, and compared with six controls treated identically apart from the surgery.
2. A mixture of amino acids was given as a prime-continuous infusion. Steady-state concentrations 75% higher than basal were attained and were maintained for 90 min. The clearances of amino acids were calculated as the ratios between amino acid infusion rate and the concentration. The urea synthesis rate was calculated as urinary excretion corrected for accumulation and intestinal loss.
3. After surgery the fasting plasma concentrations of alanine, arginine, glutamine plus glutamate, glycine, proline, lysine and threonine decreased by 20–30%, but were unchanged in the control group. The plasma clearance of α-amino nitrogen increased from 5.1 ± 1.2 ml/s before surgery (mean ± sd) to 6.1 ± 1.1 ml/s (P &lt; 0.05, paired t-test) after surgery due to increased clearances of the above-mentioned amino acids. In the control group, the clearance decreased from 6.4 ± 1.6 to 5.9 ± 1.1 (P &lt; 0.05, paired t-test). The amino acid-stimulated urea synthesis rate after surgery was 37 ± 9 μmol of N/s vs 30 ± 6 (P &lt; 0.01, paired t-test) in the controls despite a lower α-amino nitrogen concentration (4.5 ± 0.5 mmol/l vs 5.1 ± 0.5 mmol/l, P &lt; 0.05, paired t-test). The post-operative urea synthesis rate exceeded the amino nitrogen infusion by 20%.
4. Post-operatively, the insulin response to the amino acid infusion more than doubled, and the glucagon response increased by 54 %. Fasting Cortisol doubled but decreased similarly to controls during amino acid infusion.
5. After surgery amino nitrogen was cleared from the plasma pool by the liver more rapidly than it was released into the pool.
6. Our data indicate that the liver is partly responsible for the post-operative catabolism. This is not attributable to increased substrate load on the liver, but results from changed hepatic kinetics of amino nitrogen conversion. The altered hormonal responses may play a role in this condition.
Use of fractional lithium clearance in clinical and epidemiological investigation: A methodological assessment
Authors: Strazzullo P. , Iacoviello L. , Iacone R. , Giorgione N. 
Published: August 2015

1. The fractional clearance of lithium (FCLi) has been validated in the rat under controlled experimental conditions as a reliable indicator of sodium and water handling in the proximal tubule. The purpose of the present study was to evaluate some key methodological aspects related to the use of the FCLi in clinical and epidemiological investigation.
2. FCLi was determined in healthy normotensive, or in some cases, in borderline/mild essential hypertensive subjects, by a morning urine collection obtained between 09.00 and 13.00 hours after a 300 mg oral lithium carbonate load (= 8.1 mmol of elemental lithium).
3. The ratio of intra-individual to inter-individual variance of FCLi, measured in free-living subjects on unrestricted diet, was shown to be low enough (0.33) to allow adequate characterization of individuals in a population with a single measurement, or at most with two (compared with at least four measurements needed to characterize the fractional excretion of sodium).
4. The remarkable influence of dietary sodium intake on FCLi, demonstrated under metabolic ward conditions, might explain a major portion of the observed intra-individual variability.
5. At the dosage employed in the present study, oral lithium administration did not affect the renal handling of sodium, potassium or calcium. Likewise, it did not induce any change in a series of 17 metabolic parameters and indicators of renal and liver function.
6. It is concluded that the FCLi may be a safe and useful tool for the clinical and epidemiological investigation of renal sodium and water handling. The possibility of a confounding effect of dietary sodium intake, however, should be kept in mind.
Effect of glucocorticoid treatment on glucose and glutamine metabolism by the small intestine of the rat
Authors: Ardawi M. Salleh M. , Majzoub May F. , Newsholme Eric A. 
Published: August 2015

1. The effect of dexamethasone (30 μg day−1 100 g−1 body wt.) on the metabolism of glucose and glutamine was studied in the small intestine of rats after 9 days of treatment.
2. Dexamethasone treatment resulted in negative nitrogen balance (P &lt; 0.001), and produced increases in the concentrations of plasma glucose (22%, P &lt; 0.05), alanine (32%, P &lt; 0.001) and insulin (127%, P &lt; 0.001), but a decrease in the plasma concentration of glutamine (20%, P &lt; 0.05).
3. Portal-drained visceral blood flow increased by approximately 22% (P &lt; 0.001) in dexamethasone-treated rats, and was accompanied by a decrease in the arteriovenous concentration difference of glucose (43%, P &lt; 0.001) and an increase in that of lactate (22%, P &lt; 0.05), glutamine (35%, P &lt; 0.01), glutamate (33%, P &lt; 0.01) and alanine (21%, P &lt; 0.05).
4. Enterocytes isolated from dexamethasone-treated rats showed decreased and increased rates of glucose and glutamine utilization, respectively.
5. The maximal activities of hexokinase, 6-phosphofructokinase, citrate synthase and oxoglutarate dehydrogenase were decreased (30–64%, P &lt; 0.001) in intestinal mucosal scrapings of dexamethasone-treated rats, whereas the activity of glutaminase was increased (35%, P &lt; 0.001).
6. It is concluded that glucocorticoid administration decreases the rate of glucose utilization but increases that of glutamine (both in vivo and in vitro) by the epithelial cells of the small intestine. This may be caused by changes in the maximal activities of key enzymes in the pathways of glucose and glutamine metabolism in these cells.
Cardiovascular responses to stimulation of carotid baroreceptors in healthy subjects
Authors: Hainsworth R. , Al-Shamma Y. M. H. 
Published: August 2015

1. Carotid baroreceptors were stimulated by application of a subatmospheric pressure to a chamber fitted round the anterior and lateral aspects of the subject's neck (neck suction). Pulse interval and heart rate were determined from an electrocardiogram, cardiac output by a single-breath method and arterial blood pressure by an automatic sphygmomanometer.
2. The maximal prolongation of the pulse interval, determined during held expiration, occurred within 2–3 s from the onset of the neck suction. All the measured variables were in steady states between 2 and 3 min from the start of neck suction.
3. Neck suction at − 10 mmHg resulted only in an immediate change in pulse interval. All variables changed approximately linearly with the magnitude of the neck suction between − 10 and − 40 mmHg.
4. The reproducibilities of the responses to neck suction at − 30 mmHg, expressed as two standard deviations of the differences between responses on two occasions, were (mean responses in parentheses): immediate pulse interval, ± 32 (+ 236) ms; steady-state heart rate, ± 2.5 (− 6.5) beats/min; cardiac output ± 0.14 (− 0.59) 1/min; systolic and diastolic blood pressures, ± 10.0 (− 16.9) and ± 5.4 (− 10.1) mmHg, respectively.
5. Control values and responses to neck suction at − 30 mmHg were compared in subjects grouped in four age bands between 19 and 80 years. With increasing age, the control value of cardiac index (cardiac output divided by calculated body surface area) decreased, systolic and diastolic pressures increased, and the responses of all the measured variables to neck suction decreased. These results, obtained from a healthy population, provide reference values for comparison with those of individuals who may have abnormal baroreceptor reflexes.
Zinc status in inflammatory bowel disease
Authors: Ainley C. C. , Cason J. , Carlsson L. K. , Slavin B. M. , Thompson R. P. H. 
Published: August 2015

1. The zinc contents of plasma, erythrocytes, polymorphonuclear leucocytes and mononuclear leucocytes from 18 normal control subjects, 31 patients with Crohn's disease and 15 patients with ulcerative colitis were measured.
2. Plasma zinc levels were low in Crohn's disease, particularly in malnourished patients, and related to plasma albumin concentrations, but were normal in ulcerative colitis.
3. Erythrocyte zinc levels were normal in both Crohn's disease and ulcerative colitis.
4. Mean polymorphonuclear leucocyte zinc levels were normal in Crohn‘s disease and ulcerative colitis. Ten per cent of Crohn's disease patients had subnormal levels, which were associated with inactive disease, while 10% had elevated levels, which were associated with active disease. Seven per cent of ulcerative colitis patients had subnormal levels. Mononuclear leucocyte zinc levels were normal in Crohn's disease and in ulcerative colitis.
5. Tissue zinc depletion occurs in only a few patients with Crohn's disease and ulcerative colitis.
A bioenergetic explanation for the selective vulnerability of renal medullary tubules to hypoxia
Authors: Torikai Shozo 
Published: August 2015

1. In order to explain the vulnerability of medullary thick ascending limb of Heme's loop (mTAL) during hypoxia, adenosine 5′-triphosphate (ATP) content was measured in isolated rat mTAL cells during control conditions and chemically induced hypoxia and compared with those in medullary collecting duct (MCD) cells.
2. Basal ATP levels in mTAL and MCD were estimated as 3.6 and 2.1 mmol/l, respectively. Antimycin A (5 μmol/l) decreased the ATP content by 41% of the control value in the mTAL cells, but failed to reduce that of the MCD cells. Administration of sodium cyanide (5 mmol/l) drastically depleted ATP in the mTAL cells within 5 min (2–3% of control). On the other hand, ATP levels in MCD cells were sustained for at least 60 min after cyanide administration (64% of control).
3. When tubules were made permeable to sodium by the addition of nystatin, the effects of chemical hypoxia on the cell ATP levels were intensified in both segments, and this was partially blocked by pretreatment with ouabain, or by lowering the sodium concentration of the medium.
4. Higher doses of nystatin in mTAL caused a reduction in ATP levels even under control conditions, but its effect was prevented in low sodium medium.
5. The present study suggests that cell ATP levels can be altered by sodium, potassium-dependent adenosine triphosphatase activity, and that due to their high sodium-transporting activity, mTAL cells are more sensitive to reductions in ATP levels during hypoxia than are MCD cells.
Calcium and magnesium in essential hypertension
Authors: Tillman D. M. , Semple P. F. 
Published: August 2015

1. Because disturbances of calcium metabolism have been described in hypertension, measurements of plasma and serum concentrations of ionized calcium, total calcium, magnesium and renin were made in 38 patients with essential hypertension and age- and sex-matched control subjects. Urinary excretion of calcium, magnesium and sodium was also determined.
2. The mean serum concentration of ionized calcium was 1.23 ± 0.04 (sd) mmol/l in the hypertensive group and 1.21 ±0.03 mmol/l in controls, and results were similar after correction for pH. There was a weak positive correlation between serum ionized calcium (pH 7.4) and systolic pressure (r = 0.26, P &lt; 0.02), but no correlation with plasma renin concentration.
3. Although the difference between serum total calcium concentration in the hypertensive (2.29 ±0.09 mmol/l) and control (2.26 ±0.07 mmol/l) subjects was not significant, there was a significant correlation between total calcium and systolic pressure (r = 0.23, P &lt; 0.05) which was maintained after correction for other variables.
4. There were no differences in plasma concentrations of parathyroid hormone or 1,25-dihydroxycholecalciferol between hypertensive and control subjects.
5. The hypertensive group showed higher urinary excretion of calcium (5.9 ±3.0 mmol/24h) than controls (4.6 ± 1.7 mmol/24 h), but the difference was not maintained after correction for sodium excretion.
6. Serum concentrations of magnesium were similar in the two groups, but urinary excretion of magnesium was significantly lower in hypertensive (3.7 ± 1.3 mmol/24 h) than control (4.5 ±1.6 mmol/24 h) subjects and there was an inverse correlation between magnesium excretion and blood pressure (r = 0.3–0.35, P &lt; 0.01).
Sudden onset of proteinuria in chronic serum sickness in rats
Authors: Gorfien Janet B. , Van Liew Judith B. , Gorfien Stephen , Noble Bernice 
Published: August 2015

1. Daily intravenous administration of bovine serum albumin (BSA) to rats produces chronic serum sickness glomerulonephritis, an immune-complex-mediated renal disease that is eventually always fatal. We have performed a detailed study of the onset of proteinuria in chronic serum sickness in order to assess the long-term consequences of discontinuing daily BSA injections precisely at that very early and well-defined stage of disease.
2. Urine and plasma samples from rats receiving daily BSA injections were collected and analysed daily before the onset of proteinuria, at which time the rats were divided into three groups. Group 1 continued to receive daily BSA injections, in group 2 injections were stopped on the first, and in group 3 on the third, day of proteinuria. Proteinuria began suddenly and was not preceded either by microalbuminuria or abnormalities of plasma composition. The sudden expression of proteinuria was accompanied by an equally rapid development of hypoalbuminaemia and hypercholesterolaemia. Development of the characteristic glomerular histopathology of serum sickness coincided with, but did not precede, the onset of proteinuria. Despite the discontinuation of antigen injections at the onset of proteinuria, basement membrane thickening was evident 8 weeks later; proteinuria persisted and hypercholesterolaemia increased.
3. In this model of immune complex glomerulonephritis, changes in kidney function and immunopathology were abrupt and closely linked, precluding the use of those criteria to predict when proteinuria would begin. Furthermore, extremely brief periods of active immunological injury to the peripheral capillary wall were sufficient to produce persistent abnormalities of glomerular structure and function.
Luteinizing hormone in women is secreted in superimposed pulse patterns
Authors: Murdoch A. P. , Diggle P. J. , White M. C. , Harris M. , Kendall-Taylor P. , Dunlop W. 
Published: August 2015

1. The pulsatile nature of luteinizing hormone (LH) secretion has recognized physiological and clinical importance, but because of the difficulties with statistical analysis of serial data the precise nature of this pulsed signal is poorly understood. Several groups have noted small-amplitude, high-frequency pulses superimposed on large slower pulses, but, using conventional methods of analysis, it is not possible to distinguish these from assay variation or to characterize them.
2. In an alternative approach we have applied the methods of time series analysis which identify the harmonic patterns within data. Twenty-four healthy women in the early follicular phase of the cycle had blood samples taken at intervals of 1, 5 or 10 min for up to 6 h.
3. We found that LH secretion consists of superimposed harmonics of varying amplitude which occur in frequency bands of about (a) 1–3 h and (b) 2–3 min. Investigations excluded a reproducible pulsatility in our LH assay, implying that the small fast pulses are physiological events.
4. We conclude that LH release is highly complex and that the methods of time series analysis permit identification and characterization of the multiple pulses.
Effects of infusion of prostacyclin on anatomical intrapulmonary right to left shunt: a useful model of human hypoxic vasoconstriction?
Authors: Bush A. , Busst C. M. , Knight W. B. , Shinebourne E. A. 
Published: August 2015

1. Eleven infants and children (mean age 4.3 years, range 0.2–12 years) with pulmonary vascular disease secondary to congenital cardiac anomalies (n = 6) or bronchopulmonary dysplasia (n = 5), were studied during cardiac catheterization while ventilated on 100% oxygen.
2. All had a raised pulmonary vascular resistance (mean 11.8 units, range 4.1–26.0 units, normal value &lt; 3 units) and a raised anatomical intrapulmonary right to left shunt (mean 22%, range 8–50%, normal value &lt;5%). The elevated shunt was attributed to the effects of 100% oxygen and general anaesthesia causing alveolar collapse, with only partial compensation for impairment of gas exchange by compensatory local hypoxic vasoconstriction.
3. When prostacyclin was infused, pulmonary vascular resistance fell by 3.2 ± 1.8 units (mmHg litre−1 min m2), and pulmonary blood flow rose by 1.0 ± 0.7 litre min−1 m−2 (mean ± 95% confidence intervals).
4. Intrapulmonary right to left shunt fraction increased in eight of 11 patients, with a maximal rise for the group of 5.9 ± 4.6% (mean ± 95% confidence intervals). However, even at doses of prostacyclin sufficient to cause systemic vasodilatation and tachycardia, there was no evidence for a selective increase in shunt fraction.
5. We suggest that studying the effects of therapeutic interventions on intrapulmonary shunt fraction may be a useful model in vivo of human hypoxic pulmonary vasoconstriction.
Plasma dihydroxyphenylglycol for estimation of noradrenaline neuronal re-uptake in the sympathetic nervous system in vivo
Authors: Eisenhofer Graeme , Goldstein David S. , Kopin Irwin J. 
Published: August 2015

1. Neuronal re-uptake is the primary means for terminating the actions of endogenously released noradrenaline. A portion of the recaptured noradrenaline is deaminated to form dihydroxyphenylglycol. The present report describes a technique using plasma dihydroxyphenylglycol for estimation of the rate of neuronal reuptake of endogenous noradrenaline in vivo.
2. Neuronal re-uptake of noradrenaline in the sympathetic nervous system of the rat was estimated from the effects of neuronal uptake blockade with desipramine on three variables: (i) the plasma clearance of intravenously infused 3H-labelled noradrenaline, (ii) the plasma concentration of endogenous dihydroxyphenylglycol, and (iii) the plasma concentration of 3H-labelled dihydroxyphenylglycol formed from infused 3H-labelled noradrenaline.
3. Desipramine decreased plasma dihydroxyphenylglycol by 36%, this representing the fraction of dihydroxyphenylglycol in plasma that was derived from recaptured noradrenaline. After desipramine, the decrease in the rate of neuronal uptake of 3H-labelled noradrenaline was 9.7 times that of the decrease in the plasma spillover of 3H-labelled dihydroxyphenylglycol. Since the appearances in plasma of dihydroxyphenylglycol from unlabelled and 3H-labelled noradrenaline were similar, the neuronal re-uptake of endogenous noradrenaline could be assumed to be 9.7 times as much as the plasma spillover of dihydroxyphenylglycol that was derived from recaptured noradrenaline (0.15 nmol min−1 kg−1).
4. The rate of neuronal re-uptake of endogenous noradrenaline was estimated to be 1.45 nmol min−1 kg−1, whereas the plasma spillover of noradrenaline was 0.127 nmol min−1 kg−1. Thus, only a small fraction (&lt;9%) of the noradrenaline released into the synaptic cleft spills over into the circulation.
Effects of chronic hypokalaemia and adrenalectomy on potassium transport by the medullary collecting duct of the rat
Authors: Halperin M. L. , Honrath U. , Wilson D. R. , Sonnenberg H. 
Published: August 2015

1. The purpose of this study was to evaluate the roles of chronic hypokalaemia and of aldosterone in K+ transport in the medullary collecting duct. Renal clearance and duct transport measurements were made before and after KCl infusion in three groups of animals: normal rats on a regular K+ diet (group I), and sham-operated (II) or adrenalectomized rats (group III), both on a low K+ diet.
2. Only the sham-operated animals on the low K+ diet became hypokalemic. They also had the lowest rate of K+ excretion at the time of study. Adrenalectomized rats were normokalaemic, and had an intermediate rate of K+ excretion. After the acute KCl infusion, kaliuresis remained significantly depressed in the rats which were previously hypokalemic. In contrast, K+ excretion rates in response to K+ infusion were high and not significantly different in both previously normokalaemic groups, independent of the presence of the adrenal glands.
3. In the medullary collecting duct, before the KCl infusion there was no net K+ transport in either normokalaemic group (I and III). However, after the KCl infusion there was significant K+ secretion in both of these groups (32% and 22% of total urinary excretion, respectively). In contrast, the sham-operated hypokalemic rats on the low K+ diet had a small absolute, but large fractional K+ reabsorption (64% of delivered load) in the medullary collecting duct. With KCl infusion in this group, K+ delivery to the medullary duct increased, but absolute reabsorption along the duct was maintained, resulting in a fractional reabsorption of 28% of delivery.
4. The results indicate that an acute K+ load can stimulate net K+ secretion in the medullary collecting duct, and that this secretion can be independent of aldosterone. Chronic hypokalaemia stimulates net K+ reabsorption in this nephron segment, a process that persists during acute hyperkalaemia.
Increased rates of hepatic cholesterogenesis and fatty acid synthesis in septic rats in vivo: evidence for the possible involvement of insulin
Authors: de Vasconcelos Paulo R. L. , Kettlewell Michael G. W. , Gibbons Geoffrey F. , Williamson Dermot H. 
Published: August 2015

1. Sepsis induced by caecal ligation and puncture increased the rates of hepatic cholesterogenesis and fatty acid synthesis in vivo compared with sham-operated rats. These changes were accompanied by higher concentrations of lactate and pyruvate in blood and liver and an increase in plasma insulin.
2. The total activity of hydroxymethylglutarylcoenzyme A (HMG-CoA) reductase (EC 1.1.1.88) in liver was increased by sepsis, but there was no significant change in the expressed activity. Short-term insulin deficiency (induced by mannoheptulose or streptozotocin) decreased the rates of cholesterogenesis and fatty acid synthesis in livers of septic rats but did not alter the expressed/total activity of HMG-CoA reductase.
3. It is concluded that the increased rate of hepatic cholesterogenesis in septic rats is in part a result of the higher plasma insulin, the hormone acting to maintain the total activity of HMG-CoA reductase and to stimulate a step before the formation of HMG-CoA.
4. These changes may contribute to the hypertriacyl-glycerolaemia associated with sepsis.