bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma Exudation into Airways Induced by Inhaled Platelet-Activating Factor: Effect of Peptidase Inhibition
Authors: Lötvall Jan O. , Elwood Wayne , Tokuyama Kenichi , Barnes Peter J. , Chung K. Fan 
Published: August 2015

1. To evaluate whether endogenous peptide release is involved in the airway responses to inhaled platelet-activating factor, we measured lung resistance and airway microvascular leakage in anaesthetized guinea pigs pre-treated with inhalation of either saline or a combination of the peptidase inhibitors phosphoramidon (0.1 mmol/l: 60 breaths; 7.5 nmol), to inhibit neutral endopeptidase, and captopril (4.6 mmol/l: 60 breaths; 350 nmol), to inhibit angiotensin-converting enzyme.
2. Airway microvascular leakage was determined by the albumin marker Evans Blue dye injected intravenously (20 mg/kg) before platelet-activating factor or sham challenge.
3. Inhaled platelet-activating factor induced a maximum increase in lung resistance (1.43 ± 0.33 cmH2O s−1 ml−1) which was not significantly different after pretreatment with phosphoramidon and captopril (1.44 ± 0.21 cmH2O s−1 ml−1).
4. Inhalation of platelet-activating factor caused a significant increase in extravasated Evans Blue dye at all airway levels, an effect which was not potentiated by peptidase inhibition. Similar results were obtained with dye extravasated into the airway lumen and absorbed by a filter paper placed on the tracheal mucosa. Approximately 11% of the total tracheal dye was found in the lumen. There was a high correlation between tracheal tissue and tracheal lumen Evans Blue dye (r = 0.91; P &lt; 0.001).
5. We found a significantly lower dry to wet weight ratio in proximal intrapulmonary airways of animals exposed to platelet-activating factor, suggesting that platelet-activating factor caused airway oedema at this airway level.
6. Inhaled platelet-activating factor does not induce immediate release of peptides degraded by either neutral endopeptidase or angiotensin-converting enzyme in high enough quantities to cause bronchoconstriction. Inhaled platelet-activating factor may cause airway narrowing in guinea pigs largely due to plasma exudation into the airway wall and lumen.
Achlorhydria-induced hypergastrinaemia: the role of bacteria
Authors: Calam J. , Goodlad R. A. , Lee C. Y. , Ratcliffe B. , Coates M. E. , Stamp G. W. H. , Wright N. A. 
Published: August 2015

1. Studies of Helicobacter pylori show that microbes can alter gastrin release. Lack of gastric acid (achlorhydria) causes hypergastrinaemia and allows bacteria to grow within the stomach. We speculated that the bacteria contribute to the rise in gastrin seen after acid inhibition, and tested the idea by comparing plasma gastrin levels during inhibition of acid secretion between germ-free and conventional rats.
2. Matched germ-free and conventional rats (n = 8 per group) received either vehicle (saline) or one of two doses of the histamine-H2-receptor antagonist loxtidine for 1 week. Gastrin was measured in cardiac blood by a specific r.i.a.
3. Plasma gastrin concentrations in germ-free and conventional rats were 59 ± 11 pmol/l (mean ± SEM) and 36 ± 8 pmol/l, respectively, after vehicle, and 153 ± 30 pmol/l and 181 ± 27 pmol/l, respectively, after loxtidine at a dose of 10 mg day−1 kg−1, which partially inhibits acid secretion. Administration of loxtidine at a dose of 70 mg day−1 kg−1, which completely inhibits acid secretion, did not produce a significant extra rise in plasma gastrin concentration in germ-free rats (178 ± 11 pmol/l), but further elevated plasma gastrin concentrations to 278 ± 26 pmol/l in conventional rats (P &lt;0.005 compared with germ-free rats).
4. Loxtidine produced a dose-dependent rise in the number of eosinophils in the gastric mucosa of conventional rats.
5. We conclude that partial inhibition of gastric acid secretion increases gastrin release independently of bacteria, but that bacteria are involved in the further rise in gastrin which occurs on more profound inhibition of gastric acid secretion.
Adrenoceptors on blood cells from patients with primary Raynaud's phenomenon
Authors: Graafsma Sietze J. , Wollersheim Hub , Droste Herman T. , Dam Marc A. G. J. ten , van Tits Lambertus J. H. , Reyenga Joeke , de Miranda Jaap F. Rodrigues , Thien Theo 
Published: August 2015

1. α2-Adrenoceptors on platelet membranes and β2-adrenoceptors on lymphocytes were studied in 24 patients with primary Raynaud's phenomenon and in 24 age- and sex-matched control subjects. In two subgroups, a standardized mental arithmetic test and a finger-cooling test were performed.
2. Baseline blood pressure, heart rate and forearm blood flow did not differ between the two groups.
3. Baseline skin microcirculation (laser Doppler flux) was decreased in primary Raynaud's phenomenon (19 ± 15 arbitrary units) compared with control subjects (33 ± 14 arbitrary units) (P &lt;0.01).
4. Baseline plasma noradrenaline concentration (2.0011.44 versus 1.16 ± 0.36 nmol/l) and α2-adrenoceptor density (301 ± 119 versus 210 ± 82 fmol/mg) were increased in patients with primary Raynaud's phenomenon in comparison with the control subjects. The α2-adrenoceptor density/β2-adrenoceptor density ratio in patients with primary Raynaud's phenomenon was, with a value of 0.37 ± 0.04, higher than in the control subjects, where a value of 0.25 ± 0.02 was measured (P &lt;0.001). Plasma adrenaline concentration, β2-adrenoceptor density and the antagonist affinity to both receptor subtypes did not differ between both groups under baseline conditions.
5. Whereas during the finger-cooling test no differences were seen in the responses of the parameters measured, the mental arithmetic test induced an increase in laser Doppler flux in patients with primary Raynaud's phenomenon and a decrease in the control group. The increase of plasma noradrenaline concentration during the mental arithmetic test was only statistically significant in the control group.
6. The results are discussed in relation to the two common theories concerning the aetiology of primary Raynaud's phenomenon: a local vascular defect and a primary sympathetic hyperfunction.
Aldosterone, atrial natriuretic factor and sodium intake as determinants of the natriuretic response to head-out water immersion in healthy subjects
Authors: Warner Leonard C. , Morali Gilles A. , Miller Judith A. , Logan Alexander G. , Skorecki Karl L. , Blendis Laurence M. 
Published: August 2015

1. The effect of sodium intake on the natriuresis and hormonal changes induced by head-out water immersion was studied in seven normal subjects during head-out water immersion and on a control day while successively on 20 mmol of sodium/day and 100 mmol of sodium/day diets. The effects of head-out water immersion were compared with those seen on the control day for both diets.
2. The natriuresis on the 100 mmol of sodium/day diet was significantly greater than on the 20 mmol of sodium/day diet (natriuretic peak: 10.3 ± 2.2 versus 3.9 ± 1 mmol of sodium/h; P &lt; 0.01). The total sodium excretion during the 3 h of head-out water immersion was 26.2 ± 2.0 mmol on the 100 mmol of sodium/day diet and 9.9 ± 0.9 mmol on the 20 mmol of sodium/day diet (P &lt; 0.01). In contrast, the increase in the plasma atrial natriuretic factor level was similar on both diets (peak plasma atrial natriuretic factor level 23.1 ± 1.9 versus 26.2 ± 1 pg/ml; not significant). As expected, the baseline serum aldosterone level was higher on the 20 mmol of sodium/day diet and, despite a significant suppression, remained significantly higher at the end of the third hour of head-out water immersion (peak serum aldosterone level: 495 ± 130 versus 197 ± 26 pmol/l, P &lt; 0.06). Furthermore, there was an inverse relationship between the serum aldosterone level and the urinary sodium excretion at the time of peak natriuresis (r = −0.59, P &lt; 0.01).
3. We conclude that the effect of sodium intake on the natriuresis induced by head-out water immersion is more dependent upon anti-natriuretic agents, such as aldosterone, than on natriuretic factors, such as atrial natriuretic factor.
Ranitidine suppresses aluminium absorption in man
Authors: Rodger R. S. C. , Muralikrishna G. S. , Halls D. J. , Henderson J. B. , Forrest J. A. H. , MacDougall A. I. , Fell G. S. 
Published: August 2015

1. Intragastric pH monitoring was performed before and after the single-blind administration of ranitidine or placebo (saline) in eight healthy subjects and four patients with end-stage renal disease who were on regular haemodialysis.
2. The subjects were studied on two occasions and were given aluminium hydroxide (1185 mg) orally 90 min after the administration of ranitidine or saline.
3. Plasma aluminium concentrations and, in normal men, urinary excretion of aluminium were monitored before and after the oral aluminium load.
4. Intragastric pH increased significantly with ranitidine but not with placebo (P &lt; 0.001). Urinary aluminium excretion increased significantly after the administration of aluminium hydroxide during the placebo phase (P &lt; 0.001) but not during the ranitidine phase. Plasma aluminium concentrations were higher in the patients with renal failure than in the normal subjects (P &lt; 0.05), but were unchanged in both groups after the oral aluminium load.
5. This study shows that gastric pH is an important factor in the modulation of aluminium absorption in man, and indicates that reducing gastric acid secretion with ranitidine may reduce the toxicity of orally administered aluminium compounds.
A cross-sectional study of platelet cyclic AMP in healthy and hypertensive pregnant women
Authors: Horn E. H. , Cooper J. , Hardy E. , Heptinstall S. , Rubin P. C. 
Published: August 2015

1. Platelet activation in vivo occurs in healthy pregnant women and is more marked in women with preeclampsia. During pregnancy platelets have also been shown in vitro to be less susceptible to the inhibitory effects of prostacyclin. The cyclic nucleotide cyclic AMP has a key role as an inhibitory second messenger in platelets and mediates the inhibitory effects of prostacyclin.
2. We have studied cyclic AMP in relation to platelet behaviour in healthy pregnant women in the third trimester and in women with pregnancy-induced hypertension and pre-eclampsia. Non-pregnant young women were used as controls.
3. Pharmacological agents which increase levels of cyclic AMP were significantly less effective as inhibitors of platelet activation during pregnancy, but there was no difference between the healthy and hypertensive pregnant subjects.
4. Basal platelet cyclic AMP levels were the same in all three groups. However, the production of cyclic AMP in response to a range of adenylate cyclase stimulators was reduced during pregnancy, but again there was no difference between healthy and hypertensive pregnant subjects.
5. The reduction in platelet cyclic AMP levels in pregnancy occurred not only with those adenylate cyclase stimulators which operate via surface receptors, but also on direct stimulation of the enzyme with forskolin.
6. The most likely explanation of these observations is a reduction in the ability of the platelet adenylate cyclase enzyme to respond to stimulation in the third trimester of pregnancy. The consequent reduction in formation of the inhibitory second messenger cyclic AMP may in part be responsible for platelet activation in vivo during pregnancy. There does not appear to be a further difference in platelet cyclic AMP production in hypertensive pregnant women.
Glutathione depletion during experimental damage to rat skeletal muscle and its relevance to Duchenne muscular dystrophy
Authors: Jackson M. J. , Brooke M. H. , Kaiser K. , Edwards R. H. T. 
Published: August 2015

1. The release of glutathione has been studied in comparison with the release of creatine kinase from isolated rat soleus muscles subjected to certain forms of experimental damage.
2. Excessive electrically stimulated contractile activity or treatment of muscles with the mitochondrial inhibitor, 2,4-dinitrophenol, induced a substantial release of both creatine kinase and glutathione and a reduction in the total glutathione content of the muscle. The time course of this release and depletion indicates that the efflux of the two molecules is not directly related and that a reduction in muscle glutathione content does not occur before cytosolic enzyme release.
3. 2,4-Dinitrophenol-stimulated release of creatine kinase was significantly reduced by the omission of external calcium from the incubation media, but glutathione release and depletion was relatively unaffected by this. Deliberate elevation of the muscle intracellular calcium content with the calcium ionophore, A23187, induced a substantial loss of creatine kinase, but had no significant effect on the release of glutathione.
4. Muscle biopsies from patients with Duchenne muscular dystrophy were found to have an elevated content of glutathione and an equivalent protein-thiol content compared with control subjects.
5. We conclude that, although release of glutathione from skeletal muscle occurs after excessive contractile activity or inhibition of mitochondrial metabolism, this is not a key step in the damaging processes leading to cytosolic enzyme release, neither is it relevant to the ongoing damage to skeletal muscle which occurs in patients with Duchenne muscular dystrophy.
Plasma levels of an endogenous Na+–K+ pump inhibitor in relation to haemodynamic data in cardiopathic patients
Authors: Delva Pietro , Devynck Marie-Aude , Degan Maurizio , Pernollet Marie-Gabrielle , Carraroli Marco , Capra Claudio , Steele Anthony , Lechi Alessandro 
Published: August 2015

1. Despite the fact that numerous studies provide evidence for the existence of an endogenous inhibitor of the cell membrane Na+-K+ pump in plasma, little is known about the relationships between this factor and the main haemodynamic parameters.
2. In order to shed some light on this, we attempted to correlate haemodynamic parameters, measured during heart catheterization in a group of 22 cardiopathic subjects, with plasma digitalis-like activity levels, determined by two different procedures.
3. The ability of plasma to inhibit a human renal Na+-K+-ATPase showed an inverse correlation with cardiac index and a direct correlation with peripheral resistance. Plasma cross-reactivity with digoxin antibodies correlated directly with left atrial pressure.
4. These results furnish confirmation of a number of theoretical assumptions which attribute to the digitalis-like factor the ability to modify the contractility of the cardiovascular system.
Circulatory adaptation to orthostatic stress in healthy 10–14-year-old children investigated in a general practice
Authors: Dambrink J. H. A. , Imholz B. P. M. , Karemaker J. M. , Wieling W. 
Published: August 2015

1. The magnitude and time course of circulatory adaptation to active standing were investigated in healthy premenarchic girls and boys (n = 24; 10–14 years old) by non-invasive measurement of heart rate and continuous finger blood pressure (Finapres).
2. Four subjects (two girls, two boys) showed presyncopal symptoms after 4–9 min of free standing.
3. In the 20 non-fainting subjects, changes in blood pressure and heart rate upon standing did not differ between girls (n = 10) and boys (n = 10). In the initial phase of standing (first 30 s) systolic and diastolic blood pressures dropped by 22 ± 14 (mean ± sd) and 16 ± 7 mmHg, respectively, at 8 ± 2 s. Blood pressure subsequently recovered and showed an overshoot in all subjects. The transient drop in blood pressure was accompanied by an increase in heart rate of 40 ± 7 beats/min. These characteristic transient changes were not observed with passive head-up tilt. During the early steady-state phase (2 min), systolic blood pressure was similar to the supine value and diastolic blood pressure rose by 11 ± 5 mmHg. Heart rate increased by 25 ± 11 beats/min. In six of the subjects (three girls, three boys) the increase in heart rate exceeded 30 beats/min (postural tachycardia). Little further changes were observed during prolonged (10 min) standing.
4. Typical findings in the four near-fainting subjects were higher supine heart rates, no blood pressure overshoot in the initial phase (in three out of four subjects), postural tachycardia in the early steady-state phase and progressive decreases in blood pressure and heart rate afterwards.
5. In conclusion, for investigation of orthostatic circulatory adaptation in childhood it is important to pay attention to the dynamics of the circulatory response. No important differences appear to exist in orthostatic circulatory control between premenarchic girls and boys: orthostatic tachycardia and fainting appear to be common in both.
Mast cell tryptase and histamine concentrations in bronchoalveolar lavage fluid from patients with interstitial lung disease
Authors: Walls A. F. , Bennett A. R. , Godfrey R. C. , Holgate S. T. , Church M. K. 
Published: August 2015

1. Mast cell activation in the lung was investigated by measuring concentrations of mast cell tryptase and histamine in the bronchoalveolar lavage fluid from patients with bronchial carcinoma, sarcoidosis, extrinsic allergic alveolitis or cryptogenic fibrosing alveolitis and from normal subjects.
2. Histamine concentrations in bronchoalveolar lavage fluid supernatants were elevated in the bronchial carcinoma and cryptogenic fibrosing alveolitis groups, and were correlated with the histamine content of the cells recovered.
3. An avidin-biotin-enhanced antigen-capture e.l.i.s.a., using polyclonal rabbit antibody specific for tryptase, and mouse monoclonal antibody AA5, allowed the quantification of tryptase in all samples of bronchoalveolar lavage fluid. Tryptase concentrations were increased in the bronchial carcinoma and extrinsic allergic alveolitis groups and in some of the patients with sarcoidosis, and the levels correlated with mast cell numbers and also with concentrations of albumin.
4. There was no significant correlation between levels of tryptase and histamine, suggesting differences in the rates of metabolism or different cellular sources.
5. The tryptase and histamine concentrations measured suggest that there is continuous degranulation of mast cells within the normal lung, but that this process is more pronounced in patients with bronchial carcinoma or interstitial lung disease.
Local blood volume changes in women with pelvic congestion measured by applied potential tomography
Authors: Thomas D. Clive , McArdle Frank J. , Rogers Vera E. , Beard Richard W. , Brown Brian H. 
Published: August 2015

1. Applied potential tomography is a new, noninvasive technology for observing changes in blood volume. We have used it to study 12 women with lower abdominal pain caused by pelvic congestion, and 15 control subjects.
2. A significant increase in blood volume of 1.8% was observed in the pelvis of women with congestion when changing from the supine to the erect position, and of 2.7% in the control subjects (P&lt; 0.0002). The difference between the groups was not significant.
3. The distribution of the area over which blood volume changes took place was significantly different between the two groups (P&lt; 0.002). More of the posterolateral part of the pelvis was involved in women with pelvic congestion than in the control subjects.
4. Applied potential tomography distinguishes between normal women and those having pelvic congestion with a specificity of 87% and a sensitivity of 75%.
Hepatic energy status in hypotension of different aetiologies in dogs
Authors: Yokoyama Tadashi , Okamoto Ryoji , Yamamoto Yuzo , Manaka Dai , Sasaki Hirokazu , Washida Masanobu , Kitai Toshiyuki , Tanaka Akira , Yamaoka Yoshio , Kumada Kaoru , Ozawa Kazue 
Published: August 2015

1. The alterations in hepatic energy metabolism in hypotension induced by the administration of trimetaphan camsylate (Arfonad) were investigated in comparison with those produced by hypotension resulting from massive haemorrhage by measuring the arterial ketone body ratio, which reflects the hepatic mitochondrial redox state, and other indices of hepatic energy metabolism together with simultaneous measurement of hepatic blood flow in dogs.
2. Mean arterial blood pressure was decreased from 130 mmHg to 60 mmHg by the continuous intravenous infusion of trimetaphan camsylate or by the use of Wiggers' shock model. In hypotension induced by trimetaphan camsylate, the arterial ketone body ratio, ATP and total adenine nucleotide concentrations and energy charge were maintained at near-control values throughout the experimental period. By contrast, the arterial ketone body ratio decreased from 1.04 ±0.09 to 0.29 ±0.06 at 3 h after haemorrhage in Wiggers' shock model (P &lt;0.01). The ATP and total adenine nucleotide concentrations and energy charge also decreased significantly in this model (P &lt;0.05). The difference in hepatic energy status was also shown by data from 31P nuclear magnetic resonance spectroscopy.
3. During hypotension, portal venous and total hepatic blood flows diminished significantly compared with the control values in each group (P &lt;0.01). Although there was no significant difference in total hepatic flow between the two groups, the portal venous blood flow in hypotension induced by trimetaphan camsylate was significantly higher than that in Wiggers' shock model (P &lt;0.05).
4. During hypotension induced by trimetaphan camsylate, the hepatic energy metabolism was well maintained at the mean arterial blood pressure value of 60 mmHg, but in haemorrhagic hypotension it was severely curtailed, although there was no significant difference in total hepatic blood flow between the two groups. It is conjectured that the portal venous blood flow contributes significantly to the maintenance of hepatic energy metabolism and hepatic tissue perfusion during hypotension induced by trimetaphan camsylate.
Intrathoracic airstream temperatures during acute expansions of thoracic blood volume
Authors: Gilbert Ileen A. , Regnard Jacques , Lenner K. A. , Nelson J. A. , McFadden E. R. 
Published: August 2015

1. To determine the validity of employing intrathoracic heat flux as a reflection of changes in bronchial blood flow, we used a thermal probe to record airstream temperatures within the tracheobronchial tree in five normal and five asthmatic subjects during isocapnic hyperventilation challenges with and without inflation of the lower limb bladders of a pressure suit.
2. During hyperpnoea, airstream temperatures fell progressively in both subject groups. When blood volume was acutely shifted from the legs into the thorax via antishock trousers, airstream temperatures within the tracheobronchial tree rose and were significantly higher than the temperatures recorded during hyperpnoea alone. In the normal subjects, once hyperpnoea ceased, the rate of airway re-warming was similar whether or not the antishock trousers were inflated. In the asthmatic subjects, however, shifting blood into the thorax attenuated the obstructive response to hyperpnoea and slowed the rate of re-warming.
3. These data demonstrate that changes in airway blood volume are reflected in fluctuations in intrathoracic heat exchange and that disruption of the end hyperpnoea thermal gradient attenuates the airway obstruction that follows hyperpnoea. Since the bronchial blood supply is the major source of heat to the airways, this circulation may play an important role in thermally induced asthma.