bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of chronic ethanol ingestion on tissue RNA and blood flow in skeletal muscle with comparative reference to bone and tissues of the gastrointestinal tract of the rat
Authors: Preedy V. R. , Venkatesan S. , Peters T. J. , Nott D. M. , Yates J. , Jenkins S. A. 
Published: August 2015

1. The effects of feeding a diet containing ethanol as 36% of total calories for 4–5 weeks on muscle RNA content and blood flow was investigated in male rats weighing 150–250 g. Control animals were pair-fed the same diet in which ethanol was substituted by isocaloric glucose.
2. Chronic ethanol consumption reduced the capacity for type II (anaerobic, fast-twitch) fibre-rich skeletal muscles to synthesize protein as reflected by a decreased RNA/protein ratio. Type 1 (aerobic, slow-twitch) fibre-rich muscles were unaffected.
3. Ethanol feeding had no significant effect on cardiac output. Furthermore, the percentage of cardiac output to type I and type II fibre-rich muscles, bone and tissues of the gastrointestinal tract, i.e. stomach, small intestine and large intestine, was unaffected by ethanol consumption. Similarly, ethanol feeding had no effect on blood flow when it was calculated on the basis of tissue weight (ml min−1 g−1).
4. It was concluded that chronic ethanol feeding in the rat was associated with selective skeletal muscle dysfunction in the absence of changes in blood supply.
Responsiveness of superficial hand veins to adrenergic stimuli in patients with cystic fibrosis
Authors: Eichler Hans-Georg , Eichler Irmgard , Lewiston Norman , Blaschke Terrence F. , Hoffman Brian B. 
Published: August 2015

1. The basic biochemical defect of cystic fibrosis (CF) remains undetermined, but impaired function of the β-adrenoceptor-mediated adenosine 3′:5′-cyclic monophosphate (cyclic AMP)-dependent regulatory pathway in secretory cells is likely to be involved in the pathophysiology of the disease.
2. We have compared responsiveness to β-adrenergic stimulation in vivo by infusing isoprenaline locally into peripheral veins of CF patients and control subjects; the dorsal hand vein technique was used to measure the vascular response to isoprenaline.
3. CF patients required significantly higher doses of isoprenaline for half-maximal dilatation of the preconstricted veins (ED50) than controls (geometric mean: 44.5 ng/min in CF patients compared with 14.8 ng/min in controls; P &lt; 0.05). Maximal venodilatation was 74 ± 30% of baseline in CF patients compared with 94 ± 50% in controls (NS between groups).
4. The clinical score of CF patients was uncorrelated with the ED50 of isoprenaline. Thus the decreased β-adrenergic responsiveness does not seem to be related to the severity of the disease.
5. Our results indicate a defect in the cyclic-AMP-dependent pathway in vascular smooth muscle cells of CF patients. Whether this is associated with the CF gene defect itself requires further study.
Neural influences on the pulmonary vascular bed in man
Authors: Moruzzi Paolo , Sganzerla Paolo , Guazzi Maurizio D. 
Published: August 2015

1. Impedance to venous return by distention of a balloon in the inferior vena cava (IVCB) was utilized in 10 patients, during diagnostic procedures, to reduce blood flow through the lungs at baseline and to buffer its changes during stimulation of the adrenergic system, which was obtained with mental arithmetic (AT) and cold pressor (CPT) tests.
2. When venous return was unimpeded, cardiac output rose by 2.06 1/min during the AT and remained steady during the CPT, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly raised, respectively.
3. During IVCB, baseline cardiac output decreased by 710 ml/min, it rose by 925 ml/min during the AT and again remained steady during the CPT; pulmonary arteriolar resistance was unchanged from before obstruction at baseline and was significantly augmented by both tests. In particular, AT became a clear vasoconstrictor stimulus, having originally produced vasodilatation.
4. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and that vasoconstriction can be elicited in circumstances in which the flow through the lungs is restrained. The physiological importance of the neural regulation of the pulmonary circulation in man remains undefined.
Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure
Authors: Guazzi Maurizio D. , Berti Marco , Doria Elisabetta , Fiorentini Cesare , Galli Claudia , Pepi Mauro , Tamborini Gloria 
Published: August 2015

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure.
2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity.
3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines.
4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.
Effect of nedocromil sodium on down-regulation of pulmonary β-adrenoceptors
Authors: Kioumis I. , Ukena D. , Barnes Peter J. 
Published: August 2015

1. We have studied the effect of the anti-inflammatory anti-asthma drug, nedocromil sodium, on down-regulation of pulmonary β-adrenoceptors in guinea-pig lung.
2. Incubation of minced lung with isoprenaline (10 μmol/l) resulted in a reduction in maximum binding capacity of [125I]iodocyanopindolol to lung membranes from 246 ± 4 to 169 ± 6 fmol/mg of protein (mean ± sem, P &lt; 0.01, n = 18).
3. Nedocromil sodium, which had no direct effect on [125I]iodocyanopindolol binding, prevented isoprenaline-induced down-regulation, giving complete protection at a dose of 100 μmol/l.
4. The mechanism of this effect is not certain, but nedocromil sodium may interfere with the internalization of β-adrenoceptors in pulmonary parenchymal cells. This may have some therapeutic relevance.
Amiloride prevents the metabolic acidosis of a KCl load in nephrectomized rats
Authors: Altenberg Guillermo A. , Aristimuño Patricia C. , Amorena Carlos E. , Taquini Alberto C. 
Published: August 2015

1. Counter movements of K+ and H+ across cell membranes were studied in nephrectomized KCl-loaded rats. In one group of animals, the movements of K+ and H+ were determined during and after a KCl load, and in another group, amiloride was used in order to evaluate Na+ participation in K+/H+ exchange.
2. After a KCl load at constant Pco2, 79% of infused K+ left the inulin space, half of which was in exchange for H+. As a result, blood pH fell from 7.40 ± 0.01 to 7.30 ± 0.01 (mean ± sem; P &lt; 0.001).
3. During KCl infusion, the K+/H+ exchange ratio varied between 1.3 and 6.8, showing that the coupling ratio is not fixed.
4. Amiloride did not change blood pH and plasma [K+], but prevented the metabolic acidosis produced by the KCl load without affecting K+ entry into the non-inulin space. Therefore, K+ and H+ movements became completely dissociated.
5. The results indicate that KCl activates an amiloride-sensitive H+ extrusion from the cells. This finding is compatible with the view that Na+/H+ exchange participates in the metabolic acidosis produced by a KCl load.
Effects of Plasma, Tumour Necrosis Factor, Endotoxin and Dexamethasone on Extracellular Proteolysis by Neutrophils from Healthy Subjects and Patients with Emphysema
Authors: Burnett David , Chamba Anita , Hill Susan L. , Stockley Robert A. 
Published: August 2015

1. Neutrophils from patients with chronic obstructive bronchitis and emphysema or age-matched control subjects were cultured on a substrate of 125I-fibronectin. The neutrophils from patients with lung disease digested significantly more fibronectin and released more elastase into the culture supernatant than did cells from control subjects. Preincubation of neutrophils from emphysematous patients with plasma from control subjects significantly inhibited fibronectin digestion by the patients' neutrophils by, on average, 10%. Preincubation of control subjects' neutrophils with plasma from emphysematous patients had no effect on fibronectin digestion.
2. Tumour necrosis factor increased fibronectin digestion in a dose-dependent manner when the cytokine was added to the adherent cells but not when preincubated with the polymorphonuclear leucocytes in suspension. Bacterial endotoxin in concentrations above 6 μg/ml significantly increased fibronectin digestion by neutrophils, but leukotriene B4, interferon-μ and interleukin-1α had no significant effects.
3. Dexamethasone inhibited fibronectin digestion by neutrophils in a dose-dependent manner, from 11% at 10−10 mol/l to 68% at 10−3 mol/l.
Whole Body Protein Turnover and Resting Metabolic Rate in Homozygous Sickle Cell Disease
Authors: Badaloo Asha , Jackson Alan A. , Jahoor Farook 
Published: August 2015

1. Whole body protein turnover and resting metabolic rate were measured in six adults with homozygous sickle cell disease (genotype HbSS) and in six normal adults (genotype HbAA) of similar age.
2. Turnover was measured with prime/intermittent oral doses of [15N]glycine over 18 h and resting energy expenditure was measured by indirect calorimetry.
3. In HbSS, nitrogen flux (0.9 ± 0.08 g day−1 kg−1), protein synthesis (6.0 ± 0.5 g day−1 kg−1) and protein degradation (5.6 ± 0.5 g day−1 kg−1) were significantly increased compared with HbAA nitrogen (flux 0.5 ± 0.02 g day−1 kg−1, protein synthesis 3.2 ± 0.2 g day−1 kg−1 and protein degradation 2.8 ± 0.2 g day−1 kg−1).
4. Resting energy expenditure was significantly higher in HbSS compared with HbAA when expressed per unit of body weight (115 ± 3 and 94 ± 4 kJ day−1 kg−1, respectively) or weight 0.75 (317 ± 6 and 269 ± 8 kJ day−1 kg−0.75, respectively).
5. The increase in protein turnover and energy expenditure suggest that patients with HbSS exist in a hypermetabolic state that requires greater dietary energy compared with HbAA.
Vitamin D Deficiency and Muscle Strength in Male Alcoholics
Authors: Hickish T. , Colston K. W. , Bland J. M. , Maxwell J. D. 
Published: August 2015

1. Chronic alcoholism may be complicated by proximal muscle weakness associated with a selective atrophy of type II skeletal muscle fibres. The histopathological findings are non-specific as identical changes are seen in proximal muscle weakness associated with various metabolic myopathies, including osteomalacia.
2. The maximum voluntary contraction (MVC) of the dominant quadriceps and plasma 25-hydroxycholecalciferol [25-(OH)D] were measured in male alcoholics and control subjects to determine whether vitamin D deficiency contributed to proximal muscle weakness.
3. In both groups MVC declined with age and was related to body build. The distribution of plasma 25-(OH)D was skewed in alcoholics, with the mean significantly lower than in control subjects. Seventeen per cent of patients (but none of the control subjects) had pronounced biochemical deficiency [plasma 25-(OH)D &lt; 10 nmol/l].
4. Alcoholics were significantly weaker than control subjects, even after correcting for the effects of age, height and weight. The severity of associated liver disease (cirrhosis vs no cirrhosis) did not influence muscle strength. Variation in plasma 25-(OH)D and albumin made an insignificant contribution to the difference in MVC observed between patients and control subjects.
5. We conclude that proximal muscle strength is reduced in chronic alcoholism but that this is not due to associated vitamin D [25-(OH)D] deficiency or alcoholic cirrhosis.
The Antihypertensive and Renal Activities of Potassium Canrenoate are Associated with Increased Renal Prostaglandin Excretion
Authors: Castellani Sergio , Scarti Luca , Chen Ji Lin , Del Rosso Attilio , Carnovali Marino , Masotti Giulio 
Published: August 2015

1. In a double-blind, randomized, cross-over study the effects of potassium canrenoate administration (100 mg twice daily for 10 days orally) on renal prostaglandin synthesis (prostaglandin E2 and prostaglandin F2α) were evaluated in 10 normotensive females and in 10 females with essential hypertension.
2. When compared with normotensive subjects, hypertensive patients in baseline conditions showed a reduced excretion of urinary prostaglandin E2 associated with an excessive prostaglandin F2α production.
3. Potassium canrenoate significantly reduced mean blood pressure in hypertensive patients [from 118.9 ± 8.7 mmHg (1.62 ± 0.12 kPa) to a peak minimum value of 104.7 ± 9.8 mmHg (1.42 ± 0.13 kPa) on the seventh day of treatment; P &lt; 0.01 for the whole period] but not in control subjects [from 88 ± 9.4 mmHg (1.20 ± 0.13 kPa) to 84.3 ± 8.3 mmHg (1.15 ± 0.11 kPa) on the eighth day, NS] even though potassium canrenoate significantly increased sodium excretion in both groups. Renal prostaglandin excretion was affected differently in the two groups: in control subjects excretion of both prostaglandin E2 and prostaglandin F2α was increased after drug administration, whereas in hypertensive patients only prostaglandin E2 excretion was enhanced.
Cardiovascular Response to Coughing: Its Value in the Assessment of Autonomic Nervous Control
Authors: Van Lieshout E. J. , Van Lieshout J. J. , Ten Harkel A. D. J. , Wieling W. 
Published: August 2015

1. The relationship between blood pressure and heart rate responses to coughing was investigated in 10 healthy subjects in three body positions and compared with the circulatory responses to commonly used autonomic function tests: forced breathing, standing up and the Valsalva manoeuvre.
2. We observed a concomitant intra-cough increase in supine heart rate and blood pressure and a sustained post-cough elevation of heart rate in the absence of arterial hypotension. These findings indicate that the sustained increase in heart rate in response to coughing is not caused by arterial hypotension and that these heart rate changes are not under arterial baroreflex control.
3. The maximal change in heart rate in response to coughing (28 ± 8 beats/min) was comparable with the response to forced breathing (29 ± 9 beats/min, P &gt; 0.4), with a reasonable correlation (r = 0.67, P &lt; 0.05), and smaller than the change in response to standing up (41 ± 9 beats/min, P &lt; 0.01) and to the Valsalva manoeuvre (39 ± 13 beats/min, P &lt; 0.01).
4. Quantifying the initial heart rate response to coughing offers no advantage in measuring cardiac acceleratory capacity; standing up and the Valsalva manoeuvre are superior to coughing in evaluating arterial baroreflex cardiovascular function.
Effect of Almitrine on Hypoxic Ventilatory Drive Measured by Transient and Progressive Isocapnic Hypoxia in Normal Men
Authors: Airlie M. A. A. , Flenley D. C. , Warren P. M. 
Published: August 2015

1. In a double-blind placebo-controlled study, we have investigated the effect of the peripheral chemoreceptor stimulant drug almitrine bismesylate on hypoxic ventilatory drive (expressed as the slope of the minute ventilation/arterial oxygen saturation relationship in litres min−1 %−1) as measured by both progressive isocapnic hypoxia at rest and transient hypoxia (three breaths of 100% N2) during moderate exercise, in seven normal men, to determine if the ventilatory response to the transient hypoxic stimulus is a more specific measure of peripheral chemoreceptor sensitivity to hypoxia.
2. Hypoxic ventilatory drive measured using progressive isocapnic hypoxia ranged from −0.13 to −2.65 litres min−1 % −1 after placebo and from − 0.20 to − 6.48 litres min−1 %−1 after almitrine. The response was greater after almitrine in six of the seven subjects, and the difference was significant for the whole group (P &lt; 0.05).
3. Hypoxic ventilatory drive measured using transient hypoxia ranged from −0.19 to −1.59 litres min−1 %−1 after placebo and from −0.09 to −1.62 litres min−1 %−1 after almitrine. The response was not consistently greater after almitrine, and the difference was not significant for the group.
4. Difficulties in accurately quantifying a brief rise in minute ventilation after transient hypoxia, particularly in subjects with a low hypoxic ventilatory drive, may have masked small changes in the slope of the minute ventilation/arterial oxygen saturation relationship with this method. However, the significant increase in the response to progressive isocapnic hypoxia after almitrine suggests that the failure to demonstrate an effect using transient hypoxic stimuli was not solely due to between-day variation in hypoxic ventilatory drive or the small numbers of subjects studied.
5. We conclude that, although transient hypoxia avoids any central depression of ventilation that might result from the prolonged hypoxia used in the conventional steady state or progressive isocapnic methods (thereby leading to underestimation of the hypoxic ventilatory drive), the ventilatory response to such transient stimuli is also affected by factors other than peripheral chemoreceptor activity.
Effect of Vasopressin on Bronchial Reactivity to Histamine
Authors: Knox Alan J. , Britton John R. , Tattersfield Anne E. 
Published: August 2015

1. Recent evidence suggests that a high salt diet increases bronchial reactivity, but the underlying mechanism is unclear.
2. To determine whether alterations in circulating vasopressin might be responsible, we have studied the effect of an infusion of vasopressin on the airways of six normal and eight asthmatic subjects measuring the response as expiratory flow at 30% of vital capacity (V̇30P) in the normal subjects and as forced expiratory volume in 1s (FEV1) in the asthmatic subjects, in a double-blind, placebo-controlled, cross-over study.
3. Vasopressin, given as an infusion at a rate of 2 i.u./h for 1 h, followed by 4 i.u./h for a further hour, produced plasma concentrations of 12.8 and 17 ng/l, respectively, compared with 2.0 and 2.0 ng/l on placebo.
4. Airway reactivity to histamine was measured after 1 and 2 h as the provocative doses of histamine causing a 40% reduction in V̇30P (PD40V̇30P) in the normal subjects and a 20% reduction in FEV1 (PD20FEV1) in the asthmatic subjects.
5. There was a small increase in PD40V̇30P after both vasopressin and placebo in normal subjects (refractoriness) but no change in PD20FEV1 in the asthmatic subjects.
6. There was no significant difference between vasopressin and placebo in V̇30P or PD40 V̇30P over the 2 h after the drug in the normal subjects or in FEV1 or PD20FEV1 over the 2 h after the drug in the asthmatic subjects.
7. We conclude that alterations in circulating vasopressin are unlikely to be responsible for the increase in bronchial reactivity when dietary salt intake is increased.
Protoporphyrin IX-Induced Impairment of Biliary Lipid Secretion in the Rat
Authors: Perez-Barriocanal F. , Redondo-Torres J. G. , Villanueva G. R. , Arteche E. , Berenson M. M. , Marin J. J. G. 
Published: August 2015

1. In order to gain information on the effect of protoporphyrin IX on changes in the properties of the canalicular plasma membrane, we studied the release of canalicular membrane constituents, namely phospholipids, cholesterol and 5′-nucleotidase, into bile in anaesthetized rats receiving saline or taurocholate (0.5 μmol min−1 100 g−1 body weight) with or without protoporphyrin IX infusion (10 or 20 μg min−1 100 g−1 body weight).
2. Protoporphyrin IX induced an impairment of spontaneous bile flow and of biliary secretion of cholesterol, phospholipids and bile acids. The taurocholate-induced increase in bile acid output was not significantly reduced by protoporphyrin IX at either of the doses used. However, when a cholestatic dose of protoporphyrin IX was infused, the taurocholate-induced bile flow and secretion of lecithin and cholesterol were significantly reduced.
3. Biliary output of phospholipid species other than lecithin did not counterbalance the protoporphyrin IX-induced reduction in biliary lecithin secretion. Biliary outputs of both total phospholipid and lecithin were inhibited by protoporphyrin IX to similar extents.
4. Protoporphyrin IX alone had no effect on the biliary release of 5′-nucleotidase, whereas when it was given with taurocholate, it increased the bile acid-induced biliary output of this enzyme markedly.
5. In summary, these results indicate that protoporphyrin IX impairs the biliary secretion of phospholipids and cholesterol but not that of bile acid. The release of canalicular membrane constituents other than lipids was also modified by protoporphyrin IX.
The Antinatriuretic Effect of Dopaminergic Blockade during Volume Expansion is Independent of Circulating Atrial Natriuretic Factor
Authors: Coruzzi Paolo , Novarini Almerico , Musiari Luisa , Ravanetti Carlo , Ghielmi Salvatore , Rodella Anna , Montanari Alberto 
Published: August 2015

1. Ten normal subjects were subjected to 2 h water immersion with and without pharmacological dopaminergic blockade with either metoclopramide (group I) or domperidone (group II).
2. In group I, urinary sodium excretion showed a marked increase during water immersion alone, whereas it was blunted during water immersion plus dopaminergic blockade with metoclopramide (P &lt; 0.05 vs water immersion alone, n = 5). Plasma aldosterone was significantly suppressed by water immersion alone (P &lt; 0.05), but remained unchanged during water immersion plus metoclopramide. Plasma atrial natriuretic factor showed similar augmentation during water immersion alone and during water immersion plus metoclopramide.
3. Another five subjects (group II) were studied during water immersion alone and during water immersion plus dopaminergic blockade with domperidone. In this group the increase in urinary sodium excretion was similarly blunted by dopaminergic blockade. Plasma atrial natriuretic factor was equally elevated during water immersion alone and during water immersion plus domperidone, but aldosterone was suppressed by both water immersion alone and water immersion plus domperidone.
4. Our findings suggest that water immersion-induced atrial natriuretic factor release is independent of dopaminergic activity. Dopamine blockade is able to blunt significantly both water immersion-induced natriuresis and plasma aldosterone suppression, independently of the marked elevation of circulating atrial natriuretic factor, via a mechanism involving type 2 dopaminergic receptors.