bluuebunny/crossref_metadata_2025_split huggingface dataset:
Exercise training reduces the sympathetic component of the blood pressure-heart rate baroreflex in man
Authors: Kingwell Bronwyn A. , Dart Anthony M. , Jennings Garry L. , Korner Paul I. 
Published: August 2015

1. Exercise training reduces resting sympathetic activity, but the effects on sympathetic activation or withdrawal during baroreflex responses to blood pressure perturbations are controversial. The purpose of this study was to investigate the effects of training on both the vagal and sympathetic reflex heart rate responses to blood pressure changes.
2. Using 10 healthy males in a randomized cross-over design, we examined the effects of three 30 min cycling sessions at 70% of maximal capacity for 4 weeks on the steady-state reflex heart rate responses to perturbations in mean arterial pressure induced with injections of nitroprusside and phenylephrine. The method provides a sigmoidal relationship between changes in heart rate and blood pressure. The upper plateau (maximum tachycardia in response to blood pressure reduction) and lower plateau (maximum bradycardia in response to blood pressure elevation) are mainly mediated by the cardiac sympathetics and vagus, respectively. The slope of the relationship is a measure of reflex gain.
3. Training, which increased maximal oxygen consumption by 13 ± 2% (mean ± standard error of the difference), reduced supine and standing blood pressures by 3 ± 1 / 3 ± 1 mmHg (P &lt; 0.05) and 4 ± 1/2 ± 2 mmHg (P &lt; 0.05 for systolic), respectively, whereas resting heart rate was lowered by 6 ± 1 beats/min (P &lt; 0.05). Reflex sensitivity in the presence of functioning vagus and sympathetics was not altered with training, but the vagal component of sensitivity, as assessed after sympathetic blockade with propranolol, was significantly reduced. The maximal tachycardiac responses to blood pressure decreases were consistently reduced with training (sedentary, 106 beats/ min; trained, 97 ± 1 beats/min; P &lt; 0.05). This attenuation was not evident in the presence of propranolol, suggesting a sympathetic origin.
4. Exercise training thus reduced the sympathetic contribution to reflex tachycardia induced by blood pressure reduction and diminished the vagal contribution to reflex sensitivity. These effects of training may be of relevance to individuals with elevated sympathetic activity who may be at risk of myocardial ischaemia, serious ventricular arrhythmias or sudden cardiac death.
Effect of diet-induced weight loss on total body bone mass
Authors: Compston J. E. , Laskey M. A. , Croucher P. I. , Coxon A. , Kreitzman S. 
Published: August 2015

1. Total body areal bone mineral density was measured by dual-energy X-ray absorptiometry in eight women before and 10 weeks after a very-low-calorie diet [405 kcal (1701 kJ)/day].
2. The mean weight loss of 15.6 kg was accompanied by a statistically significant reduction in total body bone mineral density from 1.205 ± 0.056 to 1.175 ± 0.058 g/cm2 (mean ± sd, P &lt; 0.005).
3. After cessation of the diet, weight gradually increased and by 10 months was similar to baseline values. Total body bone mineral density also increased after stopping the diet and mean values obtained 10 months after the diet did not differ significantly from initial values. Throughout the study total body bone mineral density values in all subjects were well within the range reported for normal subjects.
4. These data indicate that diet-induced weight loss is associated with rapid bone loss, subsequent weight gain being accompanied by increases in bone mass. Further studies are required to establish the clinical significance of these findings and, in particular, the skeletal distribution of bone loss.
Accumulation of calcium by normal and dystrophin-deficient mouse muscle during contractile activity in vitro
Authors: McArdle A. , Edwards R. H. T. , Jackson M. J. 
Published: August 2015

1. Accumulation of calcium by extensor digitorum longus muscles from dystrophin-deficient mdx and control C57BL/10 mice has been studied in vitro by measurements of total muscle calcium and by following the retention of 45Ca resulting from the incubation of muscles with the isotope for up to 2 h.
2. The rate of influx of calcium, calculated from the retention of 45Ca, was linear over 2 h in muscles at rest with no significant difference between mdx and control muscles.
3. Repetitive tetanic stimuli caused a substantial increase in 45Ca flux into both mdx and control muscles. This elevated rate of influx was maintained by control muscle, but not by mdx muscle after stimulation resulting in a significantly smaller total calcium flux into mdx muscle compared with control muscle by 1 h after stimulation. Similar changes were also seen in the total muscle calcium content of mdx and control muscles. Comparison of these results with those for loss of cytosolic creatine kinase previously reported (McArdle, A., Edwards, R.H.T. & Jackson, M.J. Clin. Sci. 1991; 80, 367-71) [1] indicate that control and dystrophin-deficient muscles release equivalent amounts of intracellular creatine kinase in response to the same accumulation of intracellular calcium.
4. These results therefore do not support the hypotheses that dystrophin deficiency in muscle leads to increased calcium influx during contractile activity, or that dystrophin-deficient muscle shows any inherent increased permeability to cytosolic proteins.
Plasma platelet-activating factor degradation in patients with severe coronary artery disease
Authors: Graham Ross M. , Stephens Charlene J. , Sturm Marian J. , Taylor Roger R. 
Published: August 2015

1. Platelet-activating factor is inactivated in plasma by the action of a specific acetylhydrolase that cleaves the acetate moiety from the sn-2 position. Degradation was determined under optimized conditions and under conditions closer to those which may occur in vivo. The latter, or platelet-activating factor half-life, was measured by a modified method that is simple, inexpensive and reliable.
2. A hyperbolic relationship was found to exist between the two measures of degradation, the values in both normal subjects and patients with coronary artery disease falling on the tail of the hyperbola. Thus, there is an increase in platelet-activating factor half-life associated with a lowering of acetylhydrolase activity, but this increase is relatively small.
3. There were significant direct linear relationships between acetylhydrolase activity and serum total cholesterol and low-density-lipoprotein-cholesterol concentrations in both subject groups. Although acetylhydrolase activity was most closely associated with the low-density-lipoprotein-cholesterol fraction, the activity for a given serum level of low-density-lipoprotein-cholesterol was higher in patients with coronary artery disease.
High-voltage pulsed galvanic stimulation: effects of frequency of current on blood flow in the human calf muscle
Authors: Heath Martha E. , GIBBS Susan Bleck 
Published: August 2015

1. Twelve healthy subjects received high-voltage pulsed galvanic stimulation (115–475V d.c.) delivered in separate treatments of 2, 32 and 128 pulses/s for 10 min at the subject's maximum tolerable voltage while calf muscle blood flow was measured by non-invasive Whitney strain-gauge venous occlusion plethysmography.
2. The high-voltage pulsed galvanic stimulation was administered with negative polarity by an intermittent mode of 30 s on, 30 s off. Measurements of calf muscle blood flow were made during each 30 s period when the stimulus was off. The effect of one 30 s maximum isometric contraction of the calf muscles on blood flow was used as a standard for evaluating the effectiveness of high-voltage pulsed galvanic stimulation on calf muscle blood flow.
3. Significant (paired t-tests; P &lt; 0.05) increases in calf muscle blood flow over the preceding baseline levels occurred for the isometric contraction (322%) and for frequencies of 2 pulses/s (33.5%) and 128 pulses/s (13.36%), but not for a frequency of 32 pulses at which calf muscle blood flow increased in only six of 12 subjects. The mean increases in calf muscle blood flow at 2 and 128 pulses/s represented 11.63% and 4.0%, respectively, of that resulting from the isometric contraction.
4. A clear positive correlation between voltage level and the magnitude of increase in calf muscle blood flow was demonstrated but differed for each frequency used.
5. It is concluded that high-voltage pulsed galvanic stimulation results in a measurable increase in calf muscle blood flow when it is applied at frequencies of 2 or 128 pulses/s on intermittent mode and at maximum tolerable voltages, but the magnitude of the increase in blood flow is small compared with that stimulated by a maximal isometric contraction.
Cutaneous blood flow during a hypoglycaemic clamp in insulin-dependent diabetic patients and healthy subjects
Authors: Åman J. , Berne C. , Ewald U. , Tuvemo T. 
Published: August 2015

1. A marked cutaneous vasodilatation has been shown to occur in healthy subjects, but not in insulin-dependent diabetic patients, in response to hypoglycaemia induced by a rapid intravenous bolus injection of insulin.
2. In the present study cutaneous blood flow in response to a gradual decline in blood glucose concentration was investigated in eight young adult diabetic patients and in eight age- and sex-matched control subjects. After a hyperinsulinaemic euglycaemic clamp for 40 min, hypoglycaemia was induced (plasma glucose concentration 2 mmol/l) by a standardized stepwise reduction in the intravenous glucose infusion
3. Blood flow was measured by using a laser Doppler sensor and a cutaneous O2 electrode placed on the medial aspect of the forearm, and a laser Doppler sensor placed on the forehead.
4. No significant change in cutaneous blood flow occurred during euglycaemic hyperinsulinaemia.
5. In control subjects a marked increase in blood flow during hypoglycaemia was observed in the forearm by both methods. No corresponding change was observed in the forehead.
6. In the diabetic patients the increase in cutaneous blood flow was absent in both the forearm and forehead.
7. It is concluded that hypoglycaemia, but not hyperinsulinaemia, is associated with a regional cutaneous vasodilatation in healthy control subjects. This cutaneous vasodilatation is absent in diabetic patients.
Ion transport characteristics of the murine trachea and caecum
Authors: Smith S. N. , Alton E. W. F. W. , Geddes D. M. 
Published: August 2015

1. The basic defect in cystic fibrosis relates to abnormalities of ion transport in affected tissues, such as the respiratory and gastrointestinal tracts. The identification of the cystic fibrosis gene has enabled studies on the production of a cystic fibrosis transgenic mouse to be undertaken. Knowledge of normal ion transport will be necessary for the validation of any such animal model. We have therefore characterized selected responses of the murine trachea and caecum mounted in ‘mini’ Ussing chambers under open-circuit conditions.
2. Basal values for the trachea were: potential difference, 1.1 mV (sem 0.2; n=18); equivalent short-circuit current, 20.4 μA/cm2 (3.6); conductance, 18.2 mS/cm2 (1.7). Corresponding values for the caecum were: potential difference, 0.7 mV (0.1; n=18); equivalent short-circuit current, 11.0 μA/cm2 (1.6); conductance, 14.5 mS/cm2 (1.4).
3. Amiloride (10 μmol/l) produced a significant (P &lt; 0.001) fall in potential difference of 43.0% (5.7) in the trachea, but had no significant effect in the caecum.
4. Subsequently, one of three protocols was used to assess the capacity of either tissue for chloride secretion. Addition of a combination of forskolin (1 μmol/l) and zardaverine (10 μmol/l) produced rises in the potential difference of 873% (509) in the trachea and 399% (202) in the caecum. Both A23187 (10 μmol/l) and phorbol dibutyrate (10 nmol/l) increased tracheal potential difference by 350% (182) and 147% (47), respectively. Neither had a significant effect in the caecum.
5. Subsequent addition of bumetanide caused a fall in the stimulated potential difference of between 39.8% and 71.7%, depending on secretagogue and tissue type.
6. When a homozygous transgenic cystic fibrosis mouse becomes available, these responses should allow such an animal to be distinguished from normal or heterozygous mice.
Hepatic glutamine metabolism in the septic rat
Authors: Salleh M. , Ardawi M. 
Published: August 2015

1. The hepatic metabolism of glutamine, alanine, ammonia, urea, glutathione and glucose was studied in rats made septic by caecal ligation and puncture and was compared with that in rats that had undergone sham operation (laparotomy).
2. Sepsis resulted in increases in the plasma activities of γ-glutamyltransferase (P &lt; 0.001), alanine aminotransferase (P &lt; 0.001) and aspartate aminotransferase (P &lt; 0.001), the serum total and direct bilirubin concentrations (P &lt; 0.001), and the blood lactate (P &lt; 0.01), glutamine (P &lt; 0.05), alanine (P &lt; 0.001) and urea (P &lt; 0.05) concentrations, but produced decreases in the blood ketone body (P &lt; 0.001) and glutathione (P &lt; 0.05) concentrations and in the plasma cholesterol concentration (P &lt; 0.05). These changes were associated with marked negative nitrogen balance in septic rats.
3. Sepsis increased total hepatic blood flow (by 22.7%) together with hepatic arterial flow (by 25.8%) and portal venous flow (by 18.7%). Sepsis resulted in marked increases in the net rates of hepatic extraction of glutamine (by 164%), alanine (by 138%) and ammonia (by 259%) with concomitant increases in the net rates of hepatic release of glutamate (by 105%), glutathione (by 87.5%), glucose (by 70.1%) and urea (by 100.4%).
4. Sepsis increased the activities of liver carbamoyl-phosphate synthase (by 16.4%), ornithine transcarbamylase (by 29.8%), argininosuccinate synthase (by 28.1%) and arginase (by 33.8%).
5. Septic rats exhibited marked increases in hepatic protein (by 46.0%), RNA (by 43.4%) and DNA (by 37.7%) contents. These changes were accompanied by marked increases in the activity of thymidine kinase (by 35.9%).
6. It is concluded that the enhanced hepatic glutamine extraction in response to sepsis could be attributed to increases in hepatic ureagenesis, gluconeogenesis, proliferative and synthetic activities, and glutathione production.
Physiological basis for an animal model of the renal Fanconi syndrome: use of succinylacetone in the rat
Authors: Wyss Peter A. , Boynton Sandra B. , Chu Judith , Spencer Robert F. , Roth Karl S. 
Published: August 2015

1. The biochemical basis for the human renal Fanconi syndrome, including glucosuria, phosphaturia and aminoaciduria, remains enigmatic. This is due, in part, to the lack of an appropriate animal model. Since there is an association between the human genetic disease hereditary tyrosinaemia, for which urinary excretion of the compound succinylacetone constitutes a biochemical marker, and a renal Fanconi syndrome, we have examined the relationship between succinylacetone and renal tubular function in the rat.
2. Intraperitoneal injection of succinylacetone for 3 consecutive days into adult male Sprague-Dawley rats resulted in succinylacetone plasma concentration of 3 mmol/l. This concentration was associated with glucosuria, aminoaciduria, polyuria, reduced renal phosphate reabsorption and normal creatinine clearance. In addition, urinary porphobilinogen and total porphyrin excretions were markedly reduced. In animals permitted to recover for 7 days after succinylacetone administration, these renal functional changes remitted partially or completely. Ultrastructural examination of the kidneys after the 3 days of treatment showed no fine structural changes.
3. We conclude that the physiological alterations produced in normal rat renal tubules by succinylacetone provide the basis for the study of the biochemical changes underlying the human renal Fanconi syndrome.
Effect of l-alanine infusion on 31P nuclear magnetic resonance spectra of normal human liver: towards biochemical pathology in vivo
Authors: Dagnelie P. C. , Menon D. K. , Cox I. J. , Bell J. D. , Sargentoni J. , Coutts G. A. , Urenjak J. , Iles R. A. 
Published: August 2015

1. 31P n.m.r. spectroscopy in vivo was used to study the effect of l-alanine infusion on the concentrations of gluconeogenic intermediates in normal human liver. Studies were performed in six healthy male subjects (34–44 years, fasted overnight) using a chemical shift imaging pulse sequence on a whole-body n.m.r. system operating at 1.6T. Hepatic 31P n.m.r. spectra were obtained from 10 min before to 70 min after intravenous administration of 0.70 (n = 2), 1.40 (n = 3) or 2.80 (n = 5) nmol of l-alanine/kg body weight over 4.5 min. Concentrations of phosphomonoesters, Pi and phosphodiesters relative to ATP were calculated from peak areas in the n.m.r. spectra, using the β-ATP peak as a reference.
2. Dose-dependent spectral changes were observed for [phosphomonoesters]/[ATP] and [Pi]/[ATP]. At the highest dose given, maximal changes in [phosphomonoesters]/[ATP] (mean ± sem: 98 ± 12%, P&lt;0.005) and [Pi]/[ATP] (−33 ± 3%, P&lt;0.001) were observed approximately 45 min after the l-alanine infusion. [Phosphodiesters]/[ATP] showed a maximal increase of 24 ± 6% (P&lt;0.05), which was independent of the l-alanine dose. Hepatic ATP levels and pH did not change.
3. To identify the metabolites responsible for the changes observed in vivo, male Wistar rats were infused with 11.2 mmol of l-alanine/kg body weight. After 15 min, livers were freeze-clamped and were extracted according to standard procedures. In vitro, 31P n.m.r. spectra obtained at 8.4 or 11.7 T revealed sharp increases in the concentrations of 3-phosphoglycerate and phosphoenolpyruvate after l-alanine infusion. No significant increases in other metabolites contributing to the phosphomonoester or phosphodiester resonances in vivo were observed, suggesting that the rise in [phosphomonoesters] observed in vivo was caused by increasing concentrations of 3-phosphoglycerate, and that phosphoenolpyruvate contributed to the rise in [phosphodiesters].
5. These results show that l-alanine infusion leads to consistent changes in the 31P n.m.r. spectra of the human liver owing to increased concentrations of gluconeogenic intermediates. The ‘n.m.r.-alanine test’ may constitute a useful tool for studies of gluconeogenesis and hepatic biochemical pathology in vivo.
Absorption of non-haem iron in normal women measured by the incorporation of two stable isotopes into erythrocytes
Authors: Barrett J. F. R. , Whittaker P. G. , Williams J. G. , Lind T. 
Published: August 2015

1. Iron absorption has been quantitatively measured as the incorporation of physiological doses of stable iron isotopes into erythrocytes. Five milligrams of 57Fe (orally) and 250 μg of 58Fe (intravenously) were given to five healthy women on 2 consecutive days. Fourteen days later the changes in the 57Fe/56Fe and 58Fe/56Fe ratios in the erythrocytes of each subject were measured using an inductively coupled plasma mass spectrometer. Isotope ratios were also measured in two subjects who were not given any enriched isotope. Concomitant measurements of plasma volume using a dye-dilution technique enabled the estimation of body iron mass and the calculation of iron absorption.
2. The mean coefficients of variation for the 57Fe/56Fe ratio and the 58Fe/56Fe ratio were 0.22% and 0.47%, respectively. This precision allowed enrichments of basal ratios to be reliably detected in all cases. The mean change in the 57Fe/56Fe ratio was 0.00116 (sd 0.00052, P&lt;0.001) and the mean change in the 58Fe/56Fe ratio was 0.00035 (sd 0.00004, P&lt;0.001). Control subjects showed no enrichment.
3. The calculated iron absorption ranged from 10% to 34%, and the amount of absorption was related to the iron stores of the subjects. Percentage iron absorption was identical when estimates of the plasma volume (derived from a body mass equation) were used instead of the plasma volume determined by dye-dilution measurements. Incorporation of intravenous iron into erythrocytes was on average 81% (range 68–93%).
4. The method is especially applicable to the study of iron absorption during pregnancy when incorporation into erythrocytes cannot be predicted.
Expression of adhesion molecules on circulating leucocytes in patients with inflammatory bowel disease
Authors: Greenfield S. M. , Hamblin A. , Punchard N. A. , Thompson R. P. H. 
Published: August 2015

1. The expression of leucocyte antigens CD11/CD18 and complement receptor 1 was studied on the circulating leucocytes of 13 patients with inflammatory bowel disease and 13 age- and sex-matched healthy control subjects.
2. Monoclonal antibodies against CD11/CD18 and complement receptor 1 were added to leucocyte suspensions from patients and control subjects. Antibody binding was detected using a fluorescein-conjugated rabbit anti-mouse antibody and flow cytometry. The proportions of lymphocytes, monocytes and granulocytes expressing these molecules and the density of antigen expression, measured as mean fluorescence intensity, were determined.
3. There were no differences between patients and control subjects in the mean fluorescence intensity of antibody staining of surface molecules or in the proportion of cells expressing each molecule for any cell type. Analysis of subgroups of patients according to disease type, severity or treatment also showed no difference compared with control subjects.
4. We conclude that failure to identify a population of circulating leucocytes whose adhesion molecules or complement receptors are upregulated may arise because cells are only activated locally within the gut vasculature. Alternatively, structural changes in these molecules, rather than an increase in their number or the expression of other surface glycoproteins, may be more important in mediating adhesive interactions in inflammatory bowel disease.
Pathophysiology of unilateral high-grade carotid artery stenosis: evaluation of intracranial haemodynamics by analysis of velocity waveforms from the middle cerebral artery
Authors: Fürst Heinrich , Hartl Wolfgang H. , Jansen Ingrid , Fink Barbara , Piepgras Axel , Lauterjung Lutz , Schildberg Friedrich W. 
Published: August 2015

1. Transcranial flow velocity waves were measured via Doppler sonography of the middle cerebral artery during hypo-, hyper- and normo-capnia. Applying the principle of vascular impedance, flow velocity waves were analysed in 30 young subjects, 37 elderly subjects and 18 patients with high-grade unilateral internal carotid artery disease.
2. There was evidence that the relative peak-to-peak velocity in the middle cerebral artery could serve as an index of peripheral wave reflection and cerebral resistance (CRi). The response of CRi to changes in arterial CO2 concentration (CRi reactivity) showed a clear age-dependency. However, the absolute side-to-side asymmetry of CRi reactivity (ΔR) did not vary with age and could be used to define a normal range (0–4%CRi/vol.%CO2).
3. Selective angiography demonstrated no cerebral cross-flow through the anterior part of the circle of Willis in nine patients with carotid artery stenosis whose absolute ΔR was above the normal range and whose CRi reactivity of the affected hemisphere was lower than that of the healthy opposite hemisphere. Conversely, another group of nine patients, whose ipsilateral CRi reactivity was higher than the contralateral CRi reactivity, demonstrated cross-flow through the anterior part of the circle of Willis.
4. ΔR may be used to identify patients who have high-grade internal carotid artery stenosis and present with low cerebral vascular resistance owing to poor intracerebral collaterals.