bluuebunny/crossref_metadata_2025_split huggingface dataset:
Short-Term Variation in the Elastic Properties of a Muscular Artery in Humans
Authors: Hofstra L , Willigers J. M. , Huvers F. C. , Schaper N. C. , Kester A. D. M. , Kitslaar P. J. E. H. M. , Hoeks A. P. G. 
Published: August 2015

1. Information on the interaction between mechanical strain and the elastic properties of large arteries could give insight to the origin of haemodynamic vascular injury, possibly resulting in formation of atherosclerotic plaques. Intra-individual variation in the elastic properties of muscular arteries measured using non-invasive techniques has been observed. This variation could be due to changes in blood pressure, since the elastic properties of muscular arteries are strongly non-linear.
2. The objective of the present study was to evaluate variability in the elastic properties of a muscular artery over a time period of up to 1 h. Furthermore, the relation between changes in elastic properties and alterations in blood pressure was studied. With a non-invasive high-resolution ultrasound technique, the diameter and distension of the femoral artery were assessed by repeated measurements in 10 healthy subjects (mean age 27 ± 2.9 years) under resting conditions over 40–60 min. Intra-arterial blood pressure of the contralateral common femoral artery and heart rate were recorded simultaneously. From the distension and pulse pressure, the distension/pressure ratio was calculated, a measure of the compliance. For each parameter the variation coefficient was computed.
3. In all subjects a considerable variation was found in distension (mean variation coefficient 14.8%) but not in pulse pressure (mean variation coefficient 3.7%). The expected positive correlation between pulse pressure and distension was absent in eight subjects. As a consequence, large intra-individual variation was found in the distension/pressure ratio (mean variation coefficient 15.3%). When plotted as function of time, gradual fluctuations in the distension/pressure ratio were observed.
4. In the majority of the subjects no correlation between diastolic pressure and diameter was observed. Therefore the non-linear relation between diastolic diameter and distension cannot explain the observed variation in the distension/pressure ratio. A possible explanation might be a modification of the elastic properties of this large muscular artery by vasoactive substances and the central nervous system.
5. Under resting conditions, the elastic properties of the femoral artery in humans show large intra-individual variation with time. This variation cannot be explained by alterations in diastolic diameter, suggesting that active vessel wall behaviour is responsible for the variability. Due to the variability of the distension/pressure ratio in this large artery, a single measurement cannot give a proper characterization of the elastic properties.
Time Course of Systemic and Renal Plasma Prostanoid Concentrations and Renal Function in Ovine Hyperdynamic Sepsis
Authors: Weber Andreas , Schwieger Ian M. , Poinsot Olivier , Morel Denis R. 
Published: August 2015

1. We continuously recorded systemic and renal haemodynamic changes, and arterial, renal venous and urinary concentrations of thromboxane B2, 6-keto-prostaglandin F1α and prostaglandin E2, and determined their relationship to renal function in an ovine model of progressive hyperdynamic sepsis.
2. Nine chronically instrumented unanaesthetized sheep were given a continuous intravenous infusion of Escherichia coli endotoxin (20 ng min−1 kg−1) for 3 days.
3. Within the first 12 h of infusion, endotoxin induced a major hypotensive septic syndrome, including a persistent 30% reduction in mean arterial pressure, a 50% decrease in systemic vascular resistance and a 50% increase in mean pulmonary artery pressure, associated with severe lactacidaemia.
4. Renal blood flow decreased by 40%, and creatinine clearance, urine flow, and fractional sodium excretion decreased by more than 75%, of baseline values. After 12 h of endotoxin infusion, cardiac output increased two-fold and renal blood flow recovered to baseline values, whereas creatinine clearance remained depressed. Four sheep died between 13 and 22 h of endotoxaemia; these animals (allocated to group 1) presented a significantly and persistently more reduced renal blood flow (−23%) and creatinine clearance (−77%) after 4 h than the remaining five sheep (allocated to group 2), which survived more than 36 h (−16% and −21%, respectively), whereas systemic and pulmonary haemodynamic and gas exchange data remained similar in both groups.
5. The more pronounced decreases in renal blood flow, creatinine clearance and urine flow in group 1 were associated with higher plasma renin activity and plasma 6-keto-prostaglandin F1α concentrations and a lower fractional urinary excretion of 6-keto-prostaglandin F1α than in group 2, whereas plasma thromboxane B2 concentrations were similarly increased in both groups. Plasma prostaglandin E2 concentrations and urinary excretion were not notably affected by endotoxin infusion in either group.
6. Our results are not in favour of a significant renal production of any of these three prostanoids during endotoxaemia. In both groups, values of creatinine clearance were linearly correlated with simultaneous mean arterial pressure values after starting endotoxin infusion (group 1: creatinine clearance = 1.99 × mean arterial pressure −105, r = 0.95; group 2: creatinine clearance = 2.06 × mean arterial pressure −104, r = 0.80).
7. These findings indicate that during continuous endotoxin administration in sheep (1) the renal haemodynamic and functional responses are biphasic, (2) severe impairment of renal function is associated with elevated plasma renin activity and 6-keto-prostaglandin F1α plasma concentrations and with early fatality, and (3) renal filtration capacity directly depends on renal perfusion pressure, suggesting a loss of renal filtration autoregulation during endotoxaemia.
Changes in Regional Pulmonary Blood Flow during Lobar Bronchial Occlusion in Man
Authors: Morrell N. W. , Nijran K. S. , Biggs T. , Seed W. A. 
Published: August 2015

1. Acute hypoxic pulmonary vasoconstriction is important in the restoration of ventilation—perfusion balance in the presence of regional alveolar hypoventilation. However, the magnitude and time course of this response in man has not been adequately characterized in regions smaller than an entire lung. We have studied the effectiveness of hypoxic vasoconstriction in diverting blood from hypoxic lobes in normal supine subjects, and have documented the redistribution of pulmonary blood flow under these conditions.
2. Lobar hypoxia was induced for 80–300 s by placing occluding balloon-tipped catheters in lobar bronchi during fibreoptic bronchoscopy in 10 normal subjects. Respiratory gas partial pressures within occluded lobes were measured with a mass spectrometer. The percentage reduction in blood flow to the hypoxic lobes was assessed after injection of 99mTc-labelled albumin by γ-scintigraphy, and compared with a control scan performed 1 week later. A computer program was used to analyse changes in regional pulmonary perfusion.
3. During lobar bronchial occlusion respiratory gas partial pressures rapidly approached reported values for mixed venous partial pressures. After a mean time of occlusion of 3.5 min lobar blood flow was reduced by 47 ± 5%. During occlusions pulmonary blood flow was not evenly redistributed, but was preferentially redistributed to more cranial lung regions.
4. We conclude that acute hypoxic pulmonary vasoconstriction in occluded lobes is more effective at rapidly diverting pulmonary blood flow away from hypoxic lung regions than has previously been reported in man during unilateral hypoxia of an entire lung. Non-uniform redistribution of pulmonary blood flow in the supine subject is likely to be due to compression of the lung bases by the diaphragm in the supine position.
Urinary Endothelin-1-Like Immunoreactivity in Young Male Patients with Testicular Cancer Treated by CIS-Platinum: Comparison with other Urinary Parameters
Authors: Takeda Masayuki , Komeyama Takeshi , Tsutsui Toshiki , Mizusawa Takaki , Hideto GO , Hatano Akihiko , Tanikawa Toshiki 
Published: August 2015

1. Urinary excretion of endothelin-1-like immunoreactivity and urinary excretion of other parameters (β2-microglobulin, N-acetyl-β-d-glucosaminidase and microalbumin) were measured before, within 1 week after and 2 weeks after the administration of cis-platinum in five young male patients with testicular cancer (mean age 33.0 years) and were compared.
2. Urinary endothelin-1-like immunoreactivity/creatinine during, 1 week after, and 2 weeks after cis-platinum treatment was significantly higher than before cis-platinum. There was no difference in urinary endothelin-1-like immunoreactivity/creatinine during, 1 week after and 2 weeks after cis-platinum.
3. Among the four parameters, urinary endothelin-1-like immunoreactivity/creatinine showed the highest level after cis-platinum treatment. Urinary β2-microglobulin/creatinine most rapidly returned to normal levels after cis-platinum.
4. Although urinary endothelin-1-like immunoreactivity/creatinine did not show any significant correlations with urinary N-acetyl-β-d-glucosaminidase (r = 0.291, not significant) or urinary microalbumin/creatinine (r = 0.076, not significant), it showed a significant correlation with urinary β2-microglobulin/creatinine (r = 0.475, P &lt; 0.05).
5. These results suggest that endothelin-1 may be a sensitive urinary parameter in detecting cis-platinum-induced renal tubular injury.
Identical Effects of Indomethacin on Renal Function in Healthy Uninephrectomized Subjects and in Healthy Control Subjects
Authors: Nielsen C. B. , Sørensen S. S. , Pedersen E. B. 
Published: August 2015

1. Animal studies have shown that prostaglandins are important for renal function after unilateral nephrectomy. In order to investigate the importance of prostaglandins for renal function in the fully adapted remnant kidney in healthy uninephrectomized subjects, the acute effects of indomethacin on renal haemodynamics, lithium clearance, urinary excretion rates of prostaglandin E2, sodium and water, and plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide and arginine vasopressin were measured in 14 healthy uninephrectomized subjects (median time after nephrectomy 1.7 years) and in 14 matched healthy control subjects. In addition, nine healthy control subjects were studied without indomethacin and served as a time-control group.
2. Before indomethacin ingestion there was a significantly higher single-kidney urinary excretion rate of prostaglandin E2 in the uninephrectomized group (uninephrectomized group, 349.2 fmol/min; control group, 76.6 fmol/min; time-control group, 96.3 fmol/min).
3. Indomethacin ingestion resulted in equal changes in all parameters in both groups. These were significant decreases in glomerular filtration rate (−11.3% versus −14.6%), renal plasma flow (−6.5% versus −13.0%), urinary flow rate (−49.8% versus −49.4%), fractional sodium excretion (−44.5% versus −47.4%), lithium clearance (−33.2% versus −23.8%) and urinary excretion rate of prostaglandin E2 (−93.8% versus −86.7%) (uninephrectomized versus control subjects, values are medians). In the time-control group no changes were observed in these parameters.
4. It is concluded that healthy uninephrectomized subjects with a fully adapted remnant kidney have a normal renal response to acute indomethacin-induced inhibition of prostaglandin synthesis.
Effects of Physiological Increments in Human α-Atrial Natriuretic Peptide and Human Brain Natriuretic Peptide in Normal Male Subjects
Authors: Cheung B. M. Y. , Dickerson J. E. C. , Ashby M. J. , Brown M. J. , Brown J. 
Published: August 2015

1. Brain natriuretic peptide, closely related to atrial natriuretic peptide in structure, may be an important circulating hormone. Its physiological role is unclear. First, we studied the effects of incremental infusions of brain natriuretic peptide in six healthy men on plasma brain natriuretic peptide levels and the pharmacokinetics of brain natriuretic peptide. Synthetic human brain natriuretic peptide-32 was infused intravenously, at an initial rate of 0.4 pmol min−1 kg−1, doubling every 15 min until the dose rate reached 6.4 pmol min−1 kg−1, at which rate the infusion was maintained for 30 min.
2. The brain natriuretic peptide infusion raised the brain natriuretic peptide-like immunoreactivity from 1.4 ± 0.5 pmol/l to 21.4 ± 7.6 pmol/l. Brain natriuretic peptide-like immunoreactivity after the end of infusion was consistent with a bi-exponential decay, with half-lives of 2.1 min and 37 min.
3. Next, we studied the effects of low-dose infusion of brain natriuretic peptide to mimic physiological increments in the circulating levels in comparison with atrial natriuretic peptide. Six dehydrated male subjects received intravenous infusions of atrial natriuretic peptide and brain natriuretic peptide, separately and in combination, in a randomized double-blind, placebo-controlled, four-part cross-over design. Atrial natriuretic peptide and brain natriuretic peptide were given at the rate of 0.75 and 0.4 pmol min−1 kg−1, respectively, for 3 h. The control infusion consisted of the vehicle.
4. Analysis of variance showed that atrial natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide, but not brain natriuretic peptide alone, increased urinary flow and decreased urinary osmolality significantly. However, urinary sodium excretion was significantly increased by atrial natriuretic peptide, brain natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide.
5. None of the four infusates significantly altered the blood pressure, heart rate or glomerular filtration rate.
6. This study showed, for the first time, that physiological increments in brain natriuretic peptide, like those in atrial natriuretic peptide, are natriuretic. Although atrial natriuretic peptide and brain natriuretic peptide do not appear to interact synergistically, they are likely to act in concert in the physiological regulation of sodium balance.
Expression of Tissue Kallikrein in Human Kidney
Authors: Cumming Allan D. , Walsh Timothy , Wojtacha Davina , Fleming Stewart , Thomson David , Jenkins David A. S. 
Published: August 2015

1. We studied the distribution of human tissue kallikrein mRNA in normal and diseased kidney, using in situ hybridization, together with immunohistochemical localization of renal kallikrein protein. Materials studied were (a) normal tissue from kidneys removed because of localized renal carcinoma, (b) kidneys removed because of post-traumatic haemorrhage and (c) renal biopsy specimens from patients with membranous glomerulonephritis and nephrotic syndrome.
2. A 1.35 kb EcoRI fragment of human tissue kallikrein cDNA was labelled with [32P]dCTP using the random-primer technique, and used for in situ hybridization. A specific rabbit antibody to active human urinary kallikrein was employed for immunocytochemistry, using a peroxidase-antiperoxidase method.
3. By in situ hybridization, no tissue kallikrein gene expression was seen in the carcinoma nephrectomy specimens. Positive expression was seen in the trauma nephrectomy tissue, and in four of five nephrotic syndrome biopsies. In all kidneys, expression was confined to the renal cortex. The dominant site of gene expression was the distal tubule. Apart from one area of positive signal related to an epithelial cell of Bowman's capsule, expression was not observed in glomeruli. Expression was also seen in the walls of large- and medium-sized blood vessels.
4. By immunohistochemistry, the dominant site of immunoreactivity was the distal tubule. Dense staining was also seen in granular peripolar cells and in isolated parietal epithelial cells close to the vascular pole. Isolated immunoreactive cells were seen in the media of large- and medium-sized arteries.
5. The tissue kallikrein gene in the kidney may not be constitutively expressed, but is expressed in response to physiological or pathological stimuli. The dominant site of gene expression and tissue kallikrein localization is the distal tubule. Although kallikrein is present in granular peripolar cells in human kidney, mRNA was not located at this site. It is possible that kallikrein in these cells derives from absorption from glomerular filtrate. Tissue kallikrein mRNA and protein are present in the walls of blood vessels in human kidney. The significance of vascular kallikrein expression requires further investigation.
Plasma Adrenaline Concentration is Lower in Post-Obese than in Never-Obese Women in the Basal State, in Response to Sham-Feeding and after Food Intake
Authors: Andersen H. Bryde , Raben A. , Astrup A. , Christensen N. Juel 
Published: August 2015

1. Plasma pancreatic polypeptide, plasma catecholamine, blood glucose, plasma insulin and plasma peptide YY concentrations were studied to assess differences between eight formerly obese and eight never-obese control women during 25 min of shamfeeding (with the sight and smell of an English breakfast) and for 5 h after they had ingested the meal (3514kJ, 50% fat, 35% carbohydrate). The post-obese women had maintained their normal body weight for at least 3 months before the study.
2. The plasma noradrenaline concentration was not different between the groups either during fasting (post-obese women 0.08 ± 0.01 ng/ml versus control women 0.10 ± 0.01 ng/ml) or in the significant postprandial increase (P &lt; 0.001). The plasma adrenaline concentration increased significantly during sham-feeding in the control group from 0.024 ± 0.004 ng/ml to 0.033 ± 0.004 ng/ml (P = 0.02) in contrast with the post-obese women, who had significantly lower plasma concentrations of adrenaline in the fasting state (post-obese 0.016 ± 0.003 ng/ml versus control women 0.024 ± 0.004 ng/ml, P = 0.003), during sham-feeding (post-obese women 0.018 ± 0.002 ng/ml versus control women 0.033 ± 0.004 ng/ml, P = 0.003) and in the postprandial increase (P = 0.003). The maximal postprandial response concentrations recorded 5 h after the meal were 0.025 ± 0.003 ng/ml in post-obese women and 0.035 ± 0.004 ng/ml in control subjects (P = 0.04). There were no significant differences in plasma pancreatic polypeptide, plasma peptide YY, plasma insulin, or blood glucose concentrations between the two groups.
3. The plasma adrenaline concentration is lower in post-obese women in the basal fasting state, during sham-feeding and in response to a meal. These results indicate that post-obese subjects respond differently to food stimulation than normal subjects.
Tamm-Horsfall Mucoprotein Reduces Promotion of Calcium Oxalate Crystal Aggregation Induced by Urate in Human Urine In Vitro
Authors: Grover Phulwinder K. , Marshall Villis R. , Ryall Rosemary L. 
Published: August 2015

1. Increasing the concentration of dissolved urate promotes calcium oxalate crystallization in urine from which Tamm-Horsfall mucoprotein, an inhibitor of calcium oxalate crystal aggregation, has almost completely been removed. This study aimed to determine whether the effect of urate could be reduced or abolished by a physiological concentration of Tamm-Horsfall mucoprotein. This was approached in two ways.
2. The effect of Tamm-Horsfall mucoprotein on calcium oxalate crystallization induced by urate was tested in ultrafiltered (10 kDa) urine samples from 10 healthy men. Tamm-Horsfall mucoprotein (35 mg/l) was added to half of each specimen, the urate concentration was increased by the addition of sodium urate solution and crystallization was induced by a standard load of oxalate. The remainder of each urine specimen was used as a control; these specimens were treated with an identical amount of urate solution, but contained no Tamm-Horsfall mucoprotein. Tamm-Horsfall mucoprotein had no effect on the urinary metastable limit or on the deposition of calcium oxalate, but significantly reduced the size of the particles precipitated.
3. The effect of increasing the urate concentration in the presence of Tamm-Horsfall mucoprotein was tested. Tamm-Horsfall mucoprotein (35 mg/l) was added to 10 ultrafiltered urine samples as before, the samples were divided, and the concentration of urate was increased in half of each specimen. Compared with the control to which no urate was added, urate significantly reduced the amount of oxalate required to induce spontaneous calcium oxalate nucleation and increased the median volume and the particle size of the material deposited.
4. It was concluded that, in vivo, (a) hyperuricosuria would encourage the formation of calcium oxalate stones by promoting calcium oxalate crystallization, (b) Tamm-Horsfall mucoprotein would not lessen the effect of urate on calcium oxalate nucleation or bulk deposition but would reduce its effect on crystal aggregation; it could therefore reduce the likelihood of stone formation in patients with hyperuricosuria.
Cellular Localization of Inducible Nitric Oxide Synthase in Experimental Endotoxic Shock in the Rat
Authors: Cook H. Terence , Bune Alison J. , Jansen Albertine S. , Taylor G. Michael , Loi Rashpal K. , Cattell Victoria 
Published: August 2015

1. Endotoxin induces a shock-like syndrome with increased nitric oxide synthesis. To clarify the cellular source of NO in endotoxic shock we used immunohistochemistry and in situ hybridization to localize inducible NO synthase in rats given lipopolysaccharide or Corynebacterium parvum and lipopolysaccharide. Immunohistochemistry was carried out with an antibody raised against a synthetic peptide of mouse macrophage NO synthase. In situ hybridization was performed with 35S-labelled oligonucleotide probes corresponding to cDNA sequences common to mouse macrophage inducible NO synthase and rat vascular smooth inducible NO synthase. Monocytes and macrophages were identified by immunohistochemistry with the mouse monoclonal antibody ED1.
2. After lipopolysaccharide alone, the major site of NO synthase induction was monocytes and macrophages in multiple organs, principally liver and spleen. Bronchial, bile duct, intestinal and bladder epithelium and some hepatocytes also expressed inducible NO synthase. Expression peaked at 5 h and had returned to normal by 12 h except in spleen.
3. After priming with C. parvum, lipopolysaccharide led to a similar distribution of inducible NO synthase as lipopolysaccharide alone, but in addition there was more prominent hepatocyte staining, staining in macrophage granulomas in the liver and inducible NO synthase was present in some endothelial cells in the aorta.
4. These findings provide a direct demonstration of the cellular localization of inducible NO synthase after lipopolysaccharide.