bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abnormal vascular function and morphology in preeclampsia: a study of isolated resistance vessels
Authors: Aalkjaer C. , Danielsen H. , Johannesen P. , Pedersen E. B. , Rasmussen A. , Mulvany M. J. 
Published: August 2015

1. In order to obtain direct information about vascular changes associated with pre-eclampsia, the morphological and functional characteristics of isolated omental resistance vessels from 11 women with pre-eclampsia, 10 normotensive pregnant women and eight normotensive nonpregnant women were determined.
2. In vessels from the women with preeclampsia, the ratio of media thickness to lumen diameter was increased, compared with that in vessels from the other two groups.
3. The vessels from the women with preeclampsia had an increased responsiveness to angiotensin II and a decreased rate of relaxation, but only when compared with the vessels from the normotensive pregnant women. However, no difference in responsiveness to noradrenaline was found between any of the groups.
4. The angiotensin II responsiveness of the vessels from the women with pre-eclampsia and from the non-pregnant women were similar, suggesting that pre-eclampsia is associated with an absence of the change in vascular function which normally occurs during pregnancy.
5. The study provides direct evidence for an involvement of vascular abnormalities in the pathogenesis of pre-eclampsia.
Urinary prostaglandin E and antidiuretic hormone during water immersion in man
Authors: O'hare J. P. , Watson M. , Penney M. D. , Hampton D. , Roland J. M. , Corrall R. J. M. 
Published: August 2015

1. In 10 normal subjects water immersion to the neck at 35°C produced a highly significant natriuresis and diuresis.
2. Urinary prostaglandin E levels did not change significantly throughout immersion.
3. During the diuresis of water immersion a suppression of urinary antidiuretic hormone occurred.
Effect of induced metabolic acidosis on intracellular pH, buffer capacity and contraction force of human skeletal muscle
Authors: Hultman E. , Del Canale S. , Sjöholm H. 
Published: August 2015

1. Five volunteers were studied before and after oral administration of NH4Cl (0.3 g/kg body wt.) given in order to create a moderate acidosis.
2. The quadriceps femoris muscles were stimulated electrically for 75 s and muscle biopsies for determination of pH and metabolite content were taken before, at the end of contraction and after 10 min in the recovery period.
3. Muscle pH at rest (mean 7.04) was not significantly decreased after acidification despite an extracellular pH decrease of 0.15 unit.
4. After contraction muscle pH was significantly lower after NH4Cl. Mean values before and after acidification were 6.70 and 6.54 respectively.
5. The buffer capacity calculated as the total capacity of the muscle to buffer H+ produced during the isometric contraction before and after NH4Cl ingestion was reduced from 68.6 sl to 54.5 sl.
6. The force produced by contracting muscle was significantly lower at the end of the contraction period after NH4Cl ingestion, 44.6% of initial compared with 55.4% without NH4Cl.
Effects of acute and chronic treatment with glucocorticoids on the intestinal absorption of calcium and phosphate and on plasma 1,25-dihydroxyvitamin D levels in pigs
Authors: Fox John , Ross Richardus , Care Anthony D. 
Published: August 2015

1. We have used young pigs, each prepared surgically with a Thiry-Vella loop of proximal small intestine, to study the time course of changes in the intestinal absorption of calcium, phosphate, sodium, glucose and water and on the plasma levels of 1,25-dihydroxyvitamin D after treatment of the animals with glucocorticoids.
2. Perfusion of the intestinal loop for 6 h with a solution containing hydrocortisone or betamethasone was without effect on the absorption of calcium or phosphate.
3. The oral administration of betamethasone stimulated the absorption of calcium and phosphate by 15–20% for 2–3 days before the trend was reversed and absorption was progressively reduced.
4. Chronic treatment with betamethasone inhibited only the active component of calcium and phosphate absorption.
5. Treatment with betamethasone was associated with a sustained 25–50% increase, to a maximum by 2 days, in the absorption of sodium, glucose and water.
6. Plasma levels of 1,25-dihydroxyvitamin D were reduced within 2 days of the start of treatment and reached a minimum (40–50% decrease) in 4–6 days.
7. We conclude that the initial stimulation of calcium and phosphate absorption is caused by the increased absorption of water. The long-term decrease in absorption may not be caused solely by the decreased circulating levels of 1,25-dihydroxyvitamin D since absorption continued to fall for several weeks after 1,25-dihydroxyvitamin D levels had reached a minimum.
Obstructive jaundice blunts myocardial contractile response to isoprenaline in the dog: a clue to the susceptibility of jaundiced patients to shock?
Authors: Binah O. , Bomzon A. , Blendis L. M. , Mordohovich D. , Better O. S. 
Published: August 2015

1. Patients with obstructive jaundice are susceptible to postoperative shock. To clarify the mechanism of this phenomenon, we compared the contractile response to isoprenaline of isolated ventricular preparations from three groups of dogs: (a) dogs with chronic bile-duct ligation (CBDL), (b) dogs with choledochocaval anastomosis (CDCA) and (c) sham-operated dogs (SO).
2. Isolated ventricular muscles from CBDL and CDCA dogs showed a depressed contractile response to isoprenaline as compared with SO dogs. Mechanical performance was spared in the CBDL and CDCA dogs.
3. There were no differences in the contractile responses of SO and CBDL dogs, either to ouabain or to changes in the rates of stimulation (force-frequency relationships). These data demonstrate that, in the dog, obstructive jaundice and/or cholaemia are associated with blunted contractile response to β-adrenoreceptor stimulation in the face of intact basic mechanical performance.
4. Similar inotropic refractoriness to β-adrenoreceptor stimulation could contribute to the susceptibility to postoperative shock in patients with obstructive jaundice.
Validation of a method for measuring the short-term rate of urea synthesis after an amino acid load
Authors: Kay J. D. S. , Seakins J. W. T. , Geiseler D. , Hjelm M. 
Published: August 2015

1. The response of the plasma concentration of urea to the oral and intravenous administration of alanine was studied in healthy adult humans.
2. The instantaneous rate of urea synthesis was calculated by using a model-dependent procedure. The errors in this procedure were calculated and it was shown that analytical precision and sampling frequency, and the estimates of the distribution volume and elimination fluxes, were adequate to determine the synthesis parameters.
3. A direct test of the compartmental model was made by the intravenous injection of exogenous urea. The one-compartment model with first-order elimination gave a good fit to the experimental results at times greater than 8 min after the injection.
4. Both oral and intravenous loads of alanine had dose-dependent effects on the rate of urea synthesis. There was no evidence of a limit to the maximum possible rate of urea synthesis in these experiments and the values obtained were similar to published results for different stimuli and methods of measurement.
5. The rate of synthesis increased more rapidly after intravenous loads and subjective side-effects were less severe. The intravenous administration of alanine appears to be a suitable stimulus for urea synthesis.
Outcome of surgery for obstructive jaundice is not associated with reduced levels of plasma fibronectin
Authors: Hadjis N. S. , Griffin Susan , Blumgart L. H. , Knox P. 
Published: August 2015

1. Reduced levels of plasma fibronectin have been implicated in the septicaemia and/or endotoxaemia that can accompany trauma or burns.
2. Patients undergoing surgery for the relief of obstructive jaundice are also at risk of developing endotoxaemia or septicaemia. In this study, levels of plasma fibronectin were measured by immunoassay and bioassay in 16 such patients.
3. No patient had a significantly reduced level of plasma fibronectin. Even in the case of patients developing a fatal septicaemia and general system failure there was no significant decrease in circulating fibronectin.
4. It is concluded that measurement of plasma fibronectin is of no prognostic value and similarly infusion of fibronectin-rich cryoprecipitate would be of no therapeutic benefit.
The measurement of breathlessness induced in normal subjects: individual differences
Authors: Adams L. , Chronos N. , Lane R. , Guz A. 
Published: August 2015

1. Normal subjects show wide variability in their sensory scaling of breathlessness for equivalent degrees of ventilatory stimulation and behave ‘characteristically’ irrespective of stimulus type.
2. Observed differences are not explained by physical characteristics, ventilatory sensitivity or pattern of breathing although there is a weak association with the degree of physical fitness.
3. Differences are seen when scaling is performed with reference to both rigidly defined extremes of breathlessness (visual analogue scaling) and a subject's own relative changes in the intensity of this sensation (magnitude estimation).
4. These findings may explain the common observation, in patients with respiratory disease, of dyspnoea out of proportion to the pathophysiological state.
Erythrocyte aldehyde dehydrogenase activity in alcoholic subjects and its value as a marker for hepatic aldehyde dehydrogenase in subjects with and without liver disease
Authors: Matthewson K. , Record C. O. 
Published: August 2015

1. Erythrocyte aldehyde dehydrogenase activity was assayed in actively drinking alcoholics, patients with alcoholic liver disease who claimed to be abstaining, patients with non-alcoholic liver disorders and normal controls. Hepatic cytosolic aldehyde dehydrogenase was also assayed in the majority of the subjects.
2. Actively drinking alcoholics had significantly lower erythrocyte aldehyde dehydrogenase activity than controls (P &lt; 0.01) but abstaining alcoholic liver disease and non-alcoholic liver disorder subjects did not.
3. There was a significant correlation between erythrocyte and hepatic cytosolic aldehyde dehydrogenase activity in the control group (r = 0.94, P &lt; 0.05) but not in the other study groups.
Effect of low dose adrenaline and noradrenaline infusions on airway calibre in asthmatic patients
Authors: Berkin K. E. , Inglis G. C. , Ball S. G. , Thomson N. C. 
Published: August 2015

1. Airway, cardiovascular and metabolic responses were measured in six asthmatic patients with stable asthma during separate adrenaline, noradrenaline and control infusions. Four incremental infusion rates (4, 10, 25 and 62.5 ng min−1 kg−1) produced circulating catecholamine concentrations within the physiological range.
2. Specific airways conductance and maximal expiratory flow rates measured from complete and partial flow-volume curves increased significantly (P &lt; 0.05) during adrenaline infusion, in a dose-response manner.
3. No changes in specific airways conductance or maximal expiratory flow rates were seen during the noradrenaline or control infusion.
4. The highest adrenaline infusion rate caused a rise in systolic blood pressure (P &lt; 0.05) and plasma glucose (P &lt; 0.05) and a fall in plasma potassium (P &lt; 0.05).
5. Noradrenaline infusion caused a slight increase in diastolic blood pressure (P &lt; 0.05) but no metabolic changes. No cardiovascular or metabolic changes occurred during the control infusion.
6. Infused adrenaline, producing circulating concentrations within the physiological range, caused dose-related bronchodilatation in asthmatic patients. Circulating noradrenaline does not appear to have a role in the control of basal airway tone in asthmatic patients.
Ischaemic exercise test in myoadenylate deaminase deficiency and McArdle's disease: measurement of plasma adenosine, inosine and hypoxanthine
Authors: Sinkeler S. P. T. , Joosten E. M. G. , Wevers R. A. , Binkhorst R. A. , Oerlemans F. T. , van Bennekom C. A. , Coerwinkel M. M. , Oei T. L. 
Published: August 2015

1. Plasma adenosine, inosine and hypoxanthine concentrations were assayed in seven control subjects, five myoadenylate deaminase deficient (MADD) patients and six McArdle patients before and after ischaemic forearm exercise.
2. The plasma adenosine increase was very low in all test groups and there were no significant differences.
3. The MADD patients showed a significantly lower increase of plasma inosine and hypoxanthine after exercise as compared with the controls.
4. In the McArdle patients the increase in plasma inosine and hypoxanthine after exercise did not differ significantly from the values measured in the controls.
5. The ischaemic exercise test with measurement of plasma inosine and hypoxanthine might be of diagnostic value in MADD, but not in McArdle's disease.
Mitochondrial damage and the subcellular distribution of 2-oxoglutarate:glyoxylate carboligase in normal human and rat liver and in the liver of a patient with primary hyperoxaluria type I
Authors: Danpure C. J. , Purkiss P. , Jennings P. R. , Watts R. W. E. 
Published: August 2015

1. The subcellular distribution of 2-oxoglutarate:glyoxylate carboligase was investigated in a normal human liver, a liver from a patient with pyridoxine-resistant primary hyperoxaluria type I and rat livers subjected to various degrees and types of trauma.
2. On continuous sucrose gradients most of the carboligase fractionated with a peak equilibrium density of 1.19–1.20 g/cm3 and paralleled the distribution of the major peaks of monoamine oxidase, glutamate dehydrogenase and cytochrome oxidase and can be considered to be mitochondrial. Various proportions of the carboligase and mitochondrial marker enzymes were found to be ‘extramitochondrial’ (at or near the top of the sucrose gradients), depending on the liver source and the severity of trauma to which they were subjected.
3. Carboligase, monoamine oxidase (outer membrane marker) and glutamate dehydrogenase (matrix marker) were released from mitochondria by the homogenization and centrifugation procedures, to the extent of 19.9%, 32.4% and 11.5% respectively in hyperoxaluric liver, 12.5%, 17.9% and 8.2% in normal human liver and 3.0%, 4.9% and 3.8% in control rat liver. The proportion of extramitochondrial cytochrome oxidase (inner membrane marker) was virtually undetectable in both human and rat livers. However, sonication of rat liver homogenates or the addition of the detergent Triton X-100 caused a massive release of all four enzymes.
4. The extramitochondrial carboligase was probably in the form of a free protein of very high molecular weight or aggregate, rather than associated with a mitochondrion-derived organelle.
5. Subfractionation of a rat liver mitochondrial preparation indicated that most of the carboligase activity paralleled activities of 2-oxoglutarate decarboxylase, citrate synthase and glutamate dehydrogenase and was probably located in the matrix. The data were compatible with a previous suggestion that most of the carboligase is identical with the first decarboxylating component of the 2-oxoglutarate dehydrogenase complex. However, a significant minority of the carboligase activity showed a distribution different from that of 2-oxoglutarate decarboxylase, possibly due to structural alterations in the multi-enzyme complex.
6. We conclude that 2-oxoglutarate:glyoxylate carboligase is probably wholly mitochondrial and that the apparent cytosolic form of this enzyme is due to mitochondrial damage. Therefore previous suggestions that the lack of this component causes primary hyperoxaluria type I are no longer tenable.
Atrial natriuretic peptide inhibits the aldosterone response to angiotensin II in man
Authors: Anderson J. V. , Struthers A. D. , Payne N. N. , Slater J. D. H. , Bloom S. R. 
Published: August 2015

1. We have investigated the interaction between the recently discovered natriuretic factor alpha human atrial natriuretic peptide (alpha h-ANP) and the renin-angiotensin-aldosterone system in man.
2. Angiotensin II infused with placebo produced a significant rise of plasma aldosterone concentration (mean ± sem increment 352 ± 23 pmol/l, n = 7, P &lt; 0.001). The infusion of alpha h-ANP together with angiotensin II largely abolished the aldosterone response (P &lt; 0.001).
3. Diastolic blood pressure rose in response to the infusion of angiotensin II with placebo (mean increment 21.0 ± 0.9 mmHg, P &lt; 0.001). Systolic blood pressure increased to a lesser degree (mean increment 12.5 ± 0.7 mmHg, P &lt; 0.001).
4. The infusion of alpha h-ANP together with angiotensin II significantly blunted the diastolic pressor response (P &lt; 0.01). This ability of alpha h-ANP to blunt the pressor effect of angiotensin II may be important in the control of systemic blood pressure.
5. The inhibition of angiotensin II-stimulated aldosterone release demonstrates that alpha h-ANP may not only be a circulating natriuretic factor in its own right but that it may also act as a modulator of a related endocrine system.
Tubular reabsorption rates for myoglobin in the isolated perfused rat kidney
Authors: Ratcliffe P. J. , Esnouf M. P. , Ledingham J. G. G. 
Published: August 2015

1. The renal handling of myoglobin has been studied in the isolated perfused rat kidney.
2. Myoglobin was freely filtered. Reabsorption by the renal tubules showed saturation kinetics with a relatively low maximum rate of reabsorption (Tmax) of 27-30 μg min−1 g−1 wet wt. at a perfusate concentration of 70-80 μg/ml. Myoglobin reabsorption is therefore much less than that reported for immunoglobulin light chain or lysozyme in this model.
3. Large increases in sodium and water excretion produced by omission of oncotic agent from the perfusate did not alter the kinetics of myoglobin reabsorption.
4. The use of bovine serum albumin as oncotic agent in the perfusate prevented the tubular reabsorption of myoglobin. Small amounts of albumin are filtered by the isolated perfused kidney and it is postulated that this albumin interferes with tubular reabsorption of myoglobin.
Plasma catecholamines in pregnancy induced hypertension
Authors: Rubin Peter C. , Butters Lucy , McCabe Rosemary , Reed John L. 
Published: August 2015

1. Increased activity of the sympathetic nervous system has been implicated in the genesis of early hypertension in young people. Studies in pregnancy allow observations to be made on evolving, recently established and resolving hypertension in the human. We describe the results of two studies involving women who developed hypertension during pregnancy.
2. In the first study, plasma concentrations of noradrenaline and adrenaline were measured in 17 women with pregnancy induced hypertension (PIH) and 17 normotensive pregnant control subjects. Plasma noradrenaline (nmol/l) was lower in the PIH group compared with control patients in both semi-recumbent (1.11 ± 0.53 vs 1.98 ± 0.96, P &lt; 0.001) and standing positions (1.31 ± 0.65 vs 2.57 ± 1.27, P &lt; 0.005). Five days post partum, plasma noradrenaline had risen in the PIH group compared with pregnant values in semi-recumbent (1.65 ± 1.0 vs 1.11 ± 0.52, P &lt; 0.05) and standing positions (2.46 ± 1.5 vs 1.31 ± 0.65, P &lt; 0.05). In the normotensive patients plasma noradrenaline did not differ between post partum and pregnant values (1.51 ± 0.73 vs 1.98 ± 0.96 semi-recumbent; 2.00 ± 1.16 vs 2.57 ± 1.7 standing).
3. Logarithmic transformation of the noradrenaline concentration data resulted in a significant (P &lt; 0.02) negative correlation with diastolic blood pressure in the pregnant patients but not post partum. Plasma adrenaline concentration was the same in both groups.
4. In the second study, plasma concentrations of noradrenaline and adrenaline were measured sequentially through pregnancy in five women who developed PIH and five control subjects who remained normotensive. There was no difference in catecholamine concentrations between groups at any stage, but noradrenaline concentration tended to fall as blood pressure rose in the PIH patients.
5. We conclude that the sympathetic nervous system does not contribute to the development of PIH but responds to the increased blood pressure with decreased activity.
Pressor effect of arginine vasopressin in progressive autonomic failure
Authors: Williams T. D. M. , DaCosta D. , Mathias C. J. , Bannister R. , Lightman S. L. 
Published: August 2015

1. The blood pressure (BP) and heart rate (HR) responses to 5 min incremental intravenous infusions of noradrenaline (NA) and arginine vasopressin (AVP) were investigated both in patients with progressive autonomic failure (PAF) and in normal volunteers.
2. Stepwise infusion of NA at rates of 300–3000 pmol min−1 kg−1 produced a bradycardia and a dose related increase in BP in normal subjects. In subjects with PAF there was no significant HR response but the dose-BP response was shifted to the left with significant pressor responses at infusion rates of 60–300 pmol min−1 kg−1.
3. Stepwise infusion of AVP at 0.2–5.0 pmol min−1 kg−1 caused transient bradycardia but no pressor response in seven normal volunteers. Further increases in AVP infusion in three other subjects achieved plasma AVP levels as high as 3000–4000 pmol/l, and still no significant pressor response was observed.
4. Stepwise infusion of AVP at 0.05–2.0 pmol min−1 kg−1 in the eight subjects with PAF resulted in a pressor response without any change in HR. During this infusion plasma AVP increased from 0.8 ± 0.2 (mean ± se) to 30 ± 2 pmol/l. A significant pressor response was already apparent at a plasma AVP level of 5.5 ± 1.8 pmol/l.
Regulation of sodium-coupled phosphate transport by extracellular phosphate in cultured kidney cells (JTC-12)
Authors: Takuwa Yoh , Takeuchi Yasuhiro , Ogata Etsuro 
Published: August 2015

1. Cultured monkey kidney cells (JTC-12) have a Na+-dependent phosphate (Pi) transport system with characteristics similar to that of the renal proximal tubule. Na+-dependent Pi uptake in JTC-12 cells is affected by Pi concentrations in the culture medium. In this investigation, further characterization of this phenomenon was carried out.
2. Lowering the concentration of extracellular Pi (3.0 mmol/l to 0.3 mmol/l) induced an increase in Na+-dependent Pi uptake compared with that in control cells maintained in 3.0 mmol/l Pi whereas Na+-dependent transport of hexose and amino acid was not altered. This response was first evident at 4 h after the extracellular Pi concentration was reduced and slowly developed over the subsequent 24 h.
3. Kinetic analysis showed an increase in the Vmax without a change in the apparent Km for Pi in cells cultured in the low Pi concentration compared with control cells.
4. The response of Pi uptake was only partially prevented by cycloheximide, suggesting that both protein synthesis-dependent and -independent mechanisms are involved in the development of the response. Insulin, which has a stimulatory effect on Pi uptake in JTC-12 cells, did not affect this response.
5. These data indicate that JTC-12 cells respond to changes in extracellular Pi concentration by changing the Na+-dependent Pi uptake system. This response has a number of properties typical of the phenomenon of adaptation of renal Pi transport in vivo to dietary phosphorus load.