bluuebunny/crossref_metadata_2025_split huggingface dataset:
Changes in forearm blood flow at elevated ambient temperature and their role in the apparent impairment of glucose tolerance
Authors: Frayn K. N. , Whyte P. L. , Benson H. A. , Earl D. J. , Smith H. A. 
Published: August 2015

1. Antecubital venous plasma glucose and insulin concentrations after ingestion of 75 g of glucose were higher in six normal subjects when studied at an ambient temperature of 33°C than at an ambient temperature of 23°C; the mean area under the glucose-time curve increased from 833 at 23°C to 990 mmol min 1−1 at 33°C, that for insulin from 5300 to 7900 m-units min 1−1.
2. Core temperature was elevated by 0.5°C at 33°C ambient, although there was no marked stress response as judged by plasma levels of catecholamines, cortisol and growth hormone; at 2 h after glucose ingestion, mean noradrenaline levels were lower at 33°C than at 23°C (1.1 at 33°C vs 1.8 nmol/l at 23°C), adrenaline slightly higher (0.18 at 33°C vs 0.09 nmol/l at 23°C), cortisol and growth hormone unchanged.
3. Forearm blood flow was markedly elevated at 33°C ambient (mean total flow 9.1 at 33°C vs 1.8 ml min−1 100 ml−1 at 23°C), as were antecubital venous partial pressure of oxygen (mean 10.1 at 33°C vs 5.6 kPa at 23°C) and oxygen saturation (mean 92% at 33°C vs 70% at 23°C). There was a positive correlation between oxygen saturation and area under the glucose tolerance curve.
4. In separate experiments, arterialized glucose concentrations were measured after glucose ingestion at 23°C ambient. Antecubital venous glucose concentrations at 33°C ambient were intermediate between venous and arterialized concentrations at 23°C ambient.
5. It is concluded that the apparent impairment of glucose tolerance at elevated ambient temperature is caused at least in part by increased arterialization of the antecubital venous blood. This potential variable must be considered in research or diagnostic procedures based on the use of venous blood.
Different cation transport inhibitor in malignant renal hypertension and in uraemia
Authors: Simon Geza 
Published: August 2015

1. We investigated whether the previously reported circulating frusemide-like factor in rats with malignant renal hypertension was specific to this syndrome, or was also present in rats with chronic uraemia. 86Rb uptake (K+ transport) of monolayers of vascular smooth muscle cells was measured in the plasma of rats with malignant one-kidney, one-clip hypertension and of uraemic rats (60–70% nephrectomy).
2. Compared with control plasma, ouabain-insensitive 86Rb uptake of cells was reduced and ouabain-sensitive 86Rb uptake was unchanged in the plasma of rats with malignant hypertension. The reverse was found in the plasma of uraemic rats.
3. Inhibition of ouabain-sensitive 86Rb uptake of cells occurred in the plasma of rats with malignant hypertension when an angiotensin II antagonist was added to the reaction mixture.
4. The findings confirm the presence of a frusemide-like plasma factor in malignant hypertension and a ouabain-like plasma factor in uraemia. The presence of a ouabain-like plasma factor in malignant hypertension is camouflaged by an elevated circulating angiotensin II level, which stimulates K+ transport.
Abnormal sodium handling occurs in the isolated perfused kidney of the nephrotic rat
Authors: Firth John D. , Raine Anthony E. G. , Ledingham John G. G. 
Published: August 2015

1. In order to examine the handling of sodium by the nephrotic kidney when separated from the immediate influences of renal nerves and humoral factors, kidneys were taken from nephrotic rats (puromycin aminonucleo-side) and studied over a range of perfusion pressures using the isolated perfused kidney technique.
2. When perfused with medium containing 6.7 g/dl albumin, the nephrotic kidneys performed differently from controls with a reduction in sodium excretion at all pressures [(mean ± sem) 1.14 ± 0.43 vs 4.20 ± 0.69 μmol/min at 105 mmHg (14 kPa); 6.32 ± 1.56 vs 44.60 ± 5.30 μmol/min at 150 mmHg (20 kPa)]. Renal vascular resistance, inulin clearance, fractional sodium excretion and fractional lithium excretion were also reduced.
3. When kidneys were perfused without oncotic agent these differences between nephrotic and control kidneys remained. Perfusion with medium containing 10 g/dl albumin, designed to prevent glomerular filtration, abolished the difference in vascular resistance between the two groups. Captopril had no effect on the sodium retention or vascular resistance of nephrotic kidneys.
4. It was concluded that (a) the isolated nephrotic kidney demonstrates increased avidity for sodium, (b) the abnormality of sodium handling is not dependent on the presence of altered oncotic forces, and (c) the alteration in vascular resistance is conditional upon glomerular filtration.
Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits
Authors: May Clive N. , Whitehead Catherine J. , Heslop Kirsten E. , Mathias Christopher J. 
Published: August 2015

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium.
2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist.
3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished.
4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure.
5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation.
6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.
Effects of sodium depletion on renal prostanoid synthesis in rats: influence of the converting enzyme inhibitor captopril
Authors: Rathaus M. , Podjarny E. , Pomeranz A. , Shapira J. , Kariv N. , Bernheim J. 
Published: August 2015

1. The synthesis of prostaglandin (PG) E2, PGF2α, 6-keto-PGF1α and thromboxane (TX) B2 by isolated glomeruli, cortical tubules, inner medullary slices and outer medullary slices was measured in salt-depleted (LNa) rats and in salt-depleted rats receiving captopril (LNa-CEI). Animals were studied before and after 4, 9 and 15 days of Na+ depletion.
2. Na+ balance was reached in LNa rats after 4 days. Blood pressure and creatinine clearance remained stable. Serum Na+ decreased from 140 ± 1 to 126 ± 1 mmol/l (mean ± sem, P &lt; 0.01). In contrast, LNa-CEI rats were unable to conserve Na+ adequately: fractional excretion of Na+ and natriuresis were constantly greater than in LNa animals. As a consequence, LNa-CEI rats developed severe hyponatremia, lost weight and their creatinine clearance decreased.
3. The glomerular synthesis of PGE2, PGF2α and 6-keto-PGF1α, but not of TXB2, was significantly increased in LNa rats. In LNa-CEI rats, the synthesis of PGE2 and 6-keto-PGF1α was similar to control values, but PGF2α and TXB2 synthesis was elevated at day 9. In cortical tubules, PGE2 and PGF2α were unaffected by Na+ depletion, but 6-keto-PGF1α and TXB2 were increased and a similar trend was observed in LNa-CEI rats. In outer medulla of LNa rats, a decrease in all the eicosanoids measured was observed at day 4. In LNa-CEI animals, the synthesis of PGE2 and PGF2α, but not of 6-keto-PGF1α and TXB2, was significantly depressed. In inner medulla, Na+ depletion only tended to decrease PGF2α and 6-keto-PGF1α, but in the presence of captopril, the synthesis of all prostanoids was significantly decreased.
Regional and time-dependent effects of inflammatory mediators on airway microvascular permeability in the guinea pig
Authors: Evans T. W. , Rogers D. F. , Aursudkij B. , Chung K. F. , Barnes P. J. 
Published: August 2015

1. Airway oedema resulting from increased microvascular permeability is a characteristic pathological finding of asthma. The regional effects of putative mediators involved in asthma on airway microvascular permeability have been studied.
2. The effects of histamine, leukotriene (LT) D4 and platelet-activating factor (PAF) on microvascular permeability in the nasal mucosa, larynx, trachea, main bronchi and intrapulmonary airways of the guinea pig were assessed by measuring the extravasation of intravenously administered Evans Blue dye.
3. PAF and LTD4 caused increased microvascular leakage throughout the respiratory tract, although their effects were maximal in different regions. Histamine had no significant effect on intrapulmonary airways. PAF was more potent than LTD4 and histamine at all airway levels. For example, in the trachea the doses required to cause leakage of 50% of maximal (ED50) were 10.4 nmol/kg, 138 nmol/kg and 11.2 μmol/kg, respectively, for PAF, LTD4 and histamine.
4. The effect of the three mediators was maximal 5 min after intravenous administration. Histamine, but neither LTD4 nor PAF, still caused significant leakage 30 min after administration.
5. The increased microvascular leakage induced by the mediators was inhibited by their respective specific receptor antagonists, suggesting that the effect was mediated via specific receptors.
6. Histamine, LTD4 and PAF have varying potencies in increasing microvascular permeability in the guinea-pig respiratory tract, exert their maximal effect in different regions and have varying durations of action.
Urinary excretion of dihydroxyphenylalanine and dopamine during alterations of dietary salt intake in humans
Authors: Goldstein David S. , Stull Robin , Eisenhofer Graeme , Gill John R. 
Published: August 2015

1. Urinary excretion of dopamine (DA) increases during dietary salt loading. The majority of urinary DA is derived from circulating dihydroxyphenylalanine (dopa). Whether the increase in urinary DA excretion during salt loading results from increased efficiency of uptake of dopa by proximal tubular cells of the kidney, facilitation of intracellular conversion of dopa to DA, or increased delivery of dopa to tubular uptake sites, has been unknown.
2. In 10 inpatient normal volunteers on a constant diet, daily excretion of dopa and DA was assessed during normal sodium intake (109 mmol/day) for 1 week, low sodium intake (9 mmol/day) for 1 week and high sodium intake (249 mmol/day) for 1 week.
3. Urinary DA excretion exceeded urinary dopa excretion by about tenfold, and the excretion of both DA and dopa increased by about twofold between the low and high salt diets, with similar proportionate changes. Plasma dopa was unchanged by dietary salt manipulation.
4. The results indicate that increases in urinary DA excretion during dietary salt loading can be accounted for by increased delivery of dopa to sites of uptake by proximal tubular cells. Since dopa is released into the bloodstream by sympathetic nerve endings and by the brain, and since interference with decarboxylation of dopa attenuates natriuretic responses, dopa may function indirectly as a neurohormone involved in homoeostatic regulation of sodium balance.
Interleukin-1 potentiates the development of collagen-induced arthritis in mice
Authors: Killar L. M. , Dunn C. J. 
Published: August 2015

1. The subcutaneous administration of recombinant human interleukin-1β (rhIL-1β) was found to induce an increased incidence and earlier onset of collagen-induced arthritis in mice.
2. The rhIL-1β had different effects, depending on when it was administered after collagen-immunization.
3. The effect of rhIL-1β may be due, in part, to augmentation of the immune response to type II collagen.
4. Interleukin-1-accelerated, collagen-induced arthritis will provide a useful model for investigating the role of interleukin-1 in the regulation of arthritic diseases, and the development of anti-arthritic therapeutics.
Availability of amino acids supplied by constant intravenous infusion of synthetic dipeptides in healthy man
Authors: Albers S. , Wernerman J. , Stehle P. , Vinnars E. , Fürst P. 
Published: August 2015

1. A commercial amino acid solution supplemented with two synthetic dipeptides, l-alanyl-l-glutamine (Ala-Gln) and glycyl-l-tyrosine (Gly-Tyr), or alternatively with isonitrogenous amounts of free alanine and glycine has been continuously infused over 4 h in six apparently healthy volunteers.
2. The infusion of the solutions was not accompanied by any side effects and the volunteers reported no complaints.
3. Infusion of the alanine- and glycine-supplemented control solution resulted in an increase of the concentration of these amino acids, while no appreciable change in free glutamine concentration was observed and free tyrosine revealed a steady decrease throughout the infusion.
4. Infusion of the peptide-supplemented solution resulted in a prompt equimolar liberation of the constituent free amino acids (glutamine, alanine, tyrosine and glycine), approaching steady state after about 30 min infusion, while only trace but stable concentrations of the two dipeptides were measured throughout the infusion. No peptides were detectable in urine. The findings suggest a nearly quantitative extracellular hydrolysis of the infused dipeptides and indicate a subsequent utilization of the liberated free amino acids.
5. The estimated metabolic clearance rates and total body plasma clearances were very similar for the two dipeptides (Ala-Gln 35.9 ± 9.5 ml min−1 kg−1 and 2.9 ± 0.9 1/min, respectively; Gly-Tyr 33.7 ± 9.5 ml min−1 kg−1 and 2.7 ± 0.9 1/min, respectively); thus there is little difference in the metabolic handling of these dipeptides.
6. The study provides firm evidence that the synthetic dipeptides Ala-Gln and Gly-Tyr are quantitatively hydrolysed and that these peptides can be used as a safe and efficient source of free glutamine and tyrosine as part of a commercial solution.
Effect of parenteral nutrition on protein turnover in endotoxaemic rats
Authors: Ash S. A. , Griffin G. E. 
Published: August 2015

1. Intravenous infusion of endotoxin into rats over 18 h caused a reduction in food intake to 20% of normal levels, weight loss, hypoalbuminaemia and a fall in rates of protein synthesis in vivo in heart and skeletal muscle.
2. Measurements of protein turnover in vitro in skeletal muscle of endotoxaemic animals, showed a 50% fall in protein synthesis rates and a 200% increase in rates of protein degradation.
3. Total parenteral nutrition was only partially able to reverse endotoxin-induced weight loss. Total parenteral nutrition did not reverse endotoxin-induced catabolism in cardiac or skeletal muscle, but was able to reverse the catabolism of protein in skeletal muscle produced by starvation.
4. Endotoxin treatment elevated rates of protein synthesis in vivo in liver. The combination of parenteral nutrition and endotoxaemia further increased the rate of protein synthesis in the liver. Parenteral nutrition did not influence endotoxin-induced hypoalbuminaemia.
Doppler Characterization of the Immediate Blood Flow Velocity Pattern after Release of Prolonged Venous Occlusion of the Forearm
Authors: West J. N. W. , Salih M. S. , Littler W. A. 
Published: August 2015

1. There is a biphasic flow response measured plethysmographically after release of prolonged venous occlusion of the forearm.
2. The response consists of an early, vasodilatory, increase in flow and is followed by a decrease in flow relative to control, thought to be mediated by myogenic contraction of resistance vessels.
3. Methodological constraints with the technique of forearm plethysmography have to date precluded an individual beat-by-beat examination of this response, in particular for resolving the question of the immediate flow pattern after release of venous occlusion. It has been suggested by Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257–269] that there is a delay of up to five systolic beats before vasodilatation takes place, leading to their suggestion that the vasodilatation is passive and secondary to an increased flow through emptied capacitance vessels.
4. The introduction of peripheral Doppler techniques has led us to re-examine this response in an attempt to define short-term resistance vessel behaviour on a beat-by-beat basis.
5. Our data confirmed the hypothesis of Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257–269] that there is a constant and definite latency preceding the onset of vasodilatory flow, as reflected by changes in Doppler velocities.
Effect of the Cyclo-Oxygenase Inhibitor Fenbufen on Muscle and Liver Protein Metabolism, Muscle Glutamine and Plasma Insulin in Endotoxaemic Rats
Authors: Jepson M. M. , Millward D. J. 
Published: August 2015

1. The effect of fenbufen (γ-oxo-[1,1′-biphenyl]-4-butanoic acid), a known cyclo-oxygenase inhibitor, on the changes in muscle and liver protein metabolism in response to Escherichia coli endotoxin has been investigated in the rat.
2. Young male rats were fed a purified diet [18% (w/w) casein], with or without fenbufen (1.2 g/kg of diet). Groups of animals were injected with either endotoxin (LPS; Escherichia coli lipopolysaccharide 0.127 B8; 3 mg/kg body weight) or saline. Rectal temperature and food intake were measured over the following 24 h period, after which time measurements were made of muscle and liver protein content and synthesis in vivo, muscle protein degradation as the difference between protein synthesis and growth rates, muscle glutamine concentration and plasma insulin.
3. Fenbufen treatment alone tended to lower rectal temperature. It also reduced plasma insulin, slightly reduced food intake and slowed growth and muscle protein turnover, although muscle glutamine concentrations were unchanged. The slower protein synthesis mainly reflected reduced translational activity, which was consistent with the reduced insulin concentration.
4. LPS treatment increased rectal temperature by 1.6°C, and this was abolished by fenbufen, indicating that the dose of the drug was sufficient to block prostaglandin production in the hypothalamus.
5. LPS treatment induced similar losses in body weight and muscle protein in both control and fenbufen groups, despite a 50% lower food intake in the LPS plus fenbufen group compared with the LPS-only group. The loss of muscle protein in both groups reflected reduced protein synthesis and increased protein degradation. LPS treatment alone induced elevated plasma insulin, but fenbufen blocked this response and the insulin levels remained depressed. Muscle glutamine concentration fell in both LPS-treated groups, suggesting that the depression of protein synthesis and the development of the insulin resistance might be linked to the loss of intracellular glutamine.
6. LPS induced a relative increase in hepatic protein content, and total protein synthesis (by approximately 40%); fenbufen had no influence on these responses.
7. It is concluded that whereas treatment with fenbufen has marked effects on plasma insulin concentration, it has no influence on muscle and liver protein metabolism during endotoxaemia. Alternative mechanisms to those involving prostaglandins as mediators of the catabolic response of muscle are discussed, including those involving the glutamine transporter.
Effects of the Baroreceptor Reflex System on Atrial Natriuretic Factor Secretion during Volume Expansion in Dogs
Authors: Kohara K. , Otsuka A. , Mikami H. , Katahira K. , Tsunetoshi T. , Ogihara T. 
Published: August 2015

1. The purpose of this study was to determine whether the baroreceptor reflex system affects the secretion of atrial natriuretic factor directly or indirectly during acute volume expansion.
2. Lactated Ringer's solution containing low mol. wt. dextran was infused at 20 ml/kg for 1 h into dogs in which baroreceptors had been denervated surgically (Vx), dogs in which the autonomic system had been blocked with hexamethonium (Hx) and control dogs.
3. The plasma noradrenaline level was significantly higher in the Vx group and lower in the Hx group than in the control group throughout the experiment. The plasma levels of arginine vasopressin in the Vx and Hx groups were significantly higher than in the control group.
4. The plasma atrial natriuretic factor levels in the three groups showed similar increases during and after volume expansion.
5. The plasma atrial natriuretic factor level was significantly correlated with the right atrial pressure during volume expansion.
6. From these results, it seems unlikely that changes in the plasma level of atrial natriuretic factor during volume expansion are regulated by the baroreceptor reflex directly or indirectly by systemic changes in the sympathetic nervous system or arginine vasopressin secretion.
Atrial Natriuretic Peptide-Induced Decreases in Renal Blood Flow in Man: Implications for the Natriuretic Mechanism
Authors: Janssen Wilbert M. T. , de Zeeuw Dick , van der Hem Gjalt K. , de Jong Paul E. 
Published: August 2015

1. We studied the effect of a low-dose infusion of atrial natriuretic peptide (ANP) on renal blood flow in healthy volunteers. We additionally investigated the effect of ANP on renal haemodynamic function and on urinary sodium excretion.
2. ANP induced a rise in packed cell volume and a slight increase (but no decrease) in the renal extraction of hippuran. These changes did not offset the observed fall in effective renal plasma flow. Renal blood flow thus truly decreased and renal vascular resistance increased.
3. ANP induced an increase in glomerular filtration rate and a decrease in urinary osmolality in the first hour of ANP infusion, whereas absolute and fractional sodium excretion increased significantly only in the second hour of ANP infusion. The decrease in urinary osmolality in the first hour of ANP infusion correlated with the induced natriuresis. The changes in urinary osmolality and sodium excretion both correlated with the changes in plasma ANP levels.
4. These data indicate that ANP may cause a decrease in renal blood flow and an increase of renal vascular resistance in man. Our results suggest a role for ANP-induced (intra)renal haemodynamic changes in ANP-induced natriuresis, possibly through an increase in the filtered load of sodium into a washed-out medullary interstitium.
Circadian Rhythm of Glomerular Filtration Rate in Normal Individuals
Authors: Koopman M. G. , Koomen G. C. M. , Krediet R. T. , de Moor E. A. M. , Hoek F. J. , Arisz L. 
Published: August 2015

1. In a group of 11 normal individuals we measured glomerular filtration rate (GFR) by inulin clearances and effective renal plasma flow (ERPF) by p-aminohippurate clearances during a period of 24 h and a regimen of bedrest, identical food intake per 3 h and normal sleep/wake and light/dark cycles.
2. All subjects had a circadian rhythm for GFR with a maximum of 122 ml/min (sd 22) in the daytime, a minimum of 86 ml/min (sd 12) at night and with a relative amplitude of 33% (sd 15).
3. ERPF had a circadian rhythm with a similar relative amplitude as the GFR rhythm, but with a different phase. Because of this difference in phase, the calculated filtration fraction (GFR/ERPF) followed a circadian rhythm as well.
4. The circadian rhythms of urine volume and sodium excretion were in phase with the GFR rhythm, but the potassium rhythm had a different phase, probably because urinary potassium is largely derived from tubular secretion.
5. Urinary albumin and β2-microglobulin excretion had a circadian rhythm in phase with the GFR rhythm.
6. The highest quantity of sodium, water and β2-microglobulin was reabsorbed in the daytime; tubular reabsorption, expressed as percentage of the filtered load (fractional reabsorption), had a rhythm with a reversed phase.