bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of liver disorders on ethanol elimination and alcohol and aldehyde dehydrogenase activities in liver and erythrocytes
Authors: Zorzano Antonio , del Arbol Luis Ruiz , Herrera Emilio 
Published: August 2015

1. Liver biopsies were performed in healthy control subjects and in subjects with alcoholic and non-alcoholic liver disease in order to examine alcohol dehydrogenase (ADH; EC 1.1.1.1) and aldehyde dehydrogenase [ALDH; aldehyde dehydrogenase (NAD+); EC 1. 2. 1. 3] activities. Erythrocyte ALDH and ethanol metabolism were also investigated in the same subjects.
2. Fifteen per cent of the subjects studied (seven of 48 subjects tested) presented atypical ADH activity, characterized by elevated activity at pH 7.4 or 8.8 compared with that found in subjects with the usual ADH form. However, the ethanol elimination curves obtained in two subjects with atypical ADH were indistinguishable from the kinetics of the group with normal ADH. Subjects displaying atypical ADH activity showed normal liver and erythrocyte ALDH activities.
3. Considering only the subjects with the normal ADH form, hepatic ADH activity was unaltered in subjects with non-alcoholic liver disease (chronic hepatitis or cirrhosis) and in those with alcoholic steatosis. Subjects with alcoholic hepatitis or alcoholic cirrhosis showed a lower ADH activity compared with the healthy control group.
4. In spite of the changes detected in subjects with alcoholic liver disease, curves of blood ethanol concentration after oral administration of 0.4 g of ethanol/kg were indistinguishable between the alcoholic hepatitis group and the control group.
5. Hepatic ALDH activity, assayed at 300 μmol/l acetaldehyde, was found to be diminished in all liver pathologies investigated, regardless of their aetiology. Nevertheless, erythrocyte ALDH activity was not modified in subjects with non-alcoholic or alcoholic liver disease. As a result of these findings, no relationship was found between hepatic and erythrocyte ALDH.
6. In summary, our data demonstrate that (a) marked modifications in ADH activity, as found in patients with atypical ADH or in subjects with alcoholic liver disease, are not accompanied by parallel alterations in the kinetics of ethanol disappearance, suggesting that ADH activity per se does not limit ethanol metabolism in vivo, (b) hepatic high-Km ALDH activity is decreased in patients with liver disease independent of alcoholism, and therefore decreased ALDH activity cannot be considered as a primary defect in alcoholism but as a consequence of liver damage, and (c) erythrocyte ALDH does not reflect hepatic high-Km ALDH.
Atrial natriuretic peptide: physiological release associated with natriuresis during negative pressure breathing in man
Authors: Anderson J. V. , Maxwell D. L. , Payne N. N. , Slater J. D. H. , Bloom S. R. 
Published: August 2015

1. Negative pressure breathing was one of the first physiological tools used to study the renal effects of redistribution of the blood volume from the peripheries to the thorax. The recent discovery of a putative natriuretic hormone (atrial natriuretic peptide, ANP) in cardiac atrial tissue has rekindled interest in the effect of the cardiovascular system on renal function. We have therefore studied the effects of this physiological manoeuvre on plasma ANP concentrations and renal responses.
2. Plasma concentrations of ANP, plasma renin activity and plasma aldosterone concentration were measured during an 80 min period of negative pressure breathing at −12 cmH2O pressure in six hydrated normal subjects. Identical control studies were performed in the same subjects at at least 1 week apart.
3. Negative pressure breathing resulted in a natriuresis and diuresis which were associated with a significant rise in plasma ANP concentration. The natriuresis occurred despite an increase in plasma renin activity and in plasma aldosterone concentration.
4. These findings, under specific carefully controlled conditions, support the previously contentious postulate that negative pressure breathing enhances sodium excretion, in addition to its well-recognized diuretic effect. They add further weight to the hypothesis that expansion of the central blood volume is an important stimulus to the release of ANP from the heart (acting by way of atrial distension), and suggest that changes of plasma ANP concentration may have induced the natriuresis which occurred in the face of a modest activation of the sodium-retaining renin-aldosterone system.
Increase in Proteinuria and Reduction in Number of Anionic Sites on the Glomerular Basement Membrane in Rabbits by Infusion of Human Nephrotic Plasma in Vivo
Authors: Wilkinson Alan H. , Gillespie Cecilia , Hartley Barry , Williams D. Gwyn 
Published: August 2015

1. Intraortic suprarenal infusion in vivo of New Zealand White rabbits with plasma from patients with the nephrotic syndrome reduced the number of anionic sites labelled by the cationic polymer polyethyleneimine in the lamina rara iterna to 14.0 ± 2.7 per 1000 nm of lamina rara interna (mean ± sd) compared with 18.7 ± 2.1 (P &lt; 0.005) after infusion of plasma from normal subjects.
2. Proteinuria increased in all nine animals infused with nephrotic plasma and in two of seven infused with control plasma (P &lt; 0.01). The mean increase in proteinuria in the animals infused with nephrotic plasma was 246 mg/l (P &lt; 0.05), whereas in those infused with control plasma there was no increase.
3. We conclude that nephrotic plasma contains a factor(s) capable of neutralizing the charge of these anionic sites and concomitantly increasing proteinuria.
Effect of Phosphate-Buffered Sucrose Flush Solution upon the Initial Phase of Ischaemic Acute Renal Failure in the Rat
Authors: Ferwana O. S. , Pirie S. C. , Potts D. J. 
Published: August 2015

1. Experiments were performed upon anaesthetized rats to investigate the effect upon the initial 4 h of ischaemic acute renal failure of intrarenal flush with phosphate buffer (PB), sucrose alone and phosphate-buffered sucrose (PBS) solutions of differing compositions.
2. Kidneys flushed with PB immediately before 45 min pedicle clamp ischaemia exhibited a post-ischaemic function similar to that of control, non-flushed kidneys: they were isosthenuric and non-oliguric with a clearance of inulin (Cin) depressed to 10% of the pre-ischaemic value.
3. Kidneys flushed with 50 mmol/l sucrose in saline before ischaemia became isosthenuric, oliguric and had a more severely depressed post-ischaemic Cin compared with non-flushed kidneys.
4. Kidneys flushed with PBS containing either 50 (PBS50) or 140 (PBS140) mmol/l sucrose at pH 7 became polyuric after ischaemia, produced concentrated urine and had Cin values significantly higher than control kidneys.
5. Raising the pH of the PBS50 to 7.4 resulted in isosthenuric, polyuric kidneys that had a post-ischaemic Cin not significantly different from that of the control group.
6. It is concluded that the severity of the initial phase of ischaemic acute renal failure was significantly reduced by intrarenal flush with a PBS solution of pH 7; flush with PB or sucrose alone had no protective action.
A Comparison of Some Thermoregulatory Responses in Healthy Children and in Children with Burn Injury
Authors: Childs C. , Stoner H. B. , Little R. A. , Davenport P. J. 
Published: August 2015

1. Changes in body heat content in five normal adults, in 30 healthy children and in 24 children who had suffered burn injury 1–5 h previously, have been studied in cool (20°C) and warm (30°C) environments.
2. On moving from a cool to a warm environment, the heat content rose in both normal adults and healthy children, but the increase was significantly larger in the children.
3. Much larger changes occurred in the burned children in whom the heat content rose to a new plateau within about 8 h of the accident.
4. The changes after burn injury were unrelated to the bandaging of the burn and were little affected by the environmental temperature.
Prevention of Glucose-Induced Hypotension by the Somatostatin Analogue Octreotide (Sms 201-995) in Chronic Autonomic Failure: Haemodynamic and Hormonal Changes
Authors: Raimbach S. J. , Cortelli P. , Kooner J. S. , Bannister R. , Bloom S. R. , Mathias C. J. 
Published: August 2015

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 μg sub-cutaneously), in seven patients with chronic autonomic failure
2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged
3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase
4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.
Genetic variation on chromosome 16 is associated with abdominal aortic aneurysm
Authors: Powell Janet T. , Bashir Arshad , Dawson Sally , Vine Nicholas , Henney Adriano M. , Humphries Stephen E. , Greenhalgh Roger M. 
Published: August 2015

1. There is a familial tendency to abdominal aortic aneurysms. We have followed up a previous report of a weak association between the haptoglobin 2-1 phenotype and aortic aneurysm and investigated polymorphisms of the haptoglobin gene and neighbouring cholesterol ester transfer protein gene on the long arm of chromosome 16 in patients with atherosclerotic abdominal aortic aneurysm, patients with stenosing aortic atherosclerosis and healthy control subjects. The protein polymorphism of haptoglobin results from variant α-chains, α1 and α2, the phenotype nomenclature describing the two α-chains. We have also investigated whether the different haptoglobin phenotypes influence the degradation of aortic connective tissue.
2. The frequency of the haptoglobin α1 allele was increased in patients with aneurysms compared with healthy control subjects (0.51 versus 0.35, P &lt; 0.05). Patients homozygous for the α2 allele had the highest mean age at aneurysm resection. The frequency of a rare polymorphism at the cholesterol ester transfer protein locus was also increased in aneurysm patients (0.15 versus 0.05 in control subjects, P &lt; 0.01). These two genetic markers appear to act independently. Haptoglobins containing an α1-chain accelerated two-to fourfold the degradation by elastases of aortic elastin in vitro.
3. Genetic variation in the haptoglobin and cholesterol ester transfer protein genes appears to influence dilatation of the abdominal aorta. Variation at the haptoglobin locus could have a direct effect on the degradation of elastin in atherosclerotic aorta, whereas variation at the cholesterol ester transfer protein locus could affect lipid metabolism and promote atherosclerosis. These results indicate that a gene on chromosome 16 is associated with aortic aneurysm, although this may be an as yet unidentified gene in linkage disequilibrium with the haptoglobin and cholesterol ester transfer protein genes.
Pre-replicative phase-related changes in bile acid-induced choleresis in the regenerating rat liver
Authors: Garcia-Marin J. J. , Regueiro P. , Perez-Antona J. C. , Villanueva G. R. , Perez-Barriocanal F. 
Published: August 2015

1. During the pre-replicative phase of the regenerating rat liver some interesting changes occur, which might selectively modify some mechanisms involved in bile formation, such as those responsible for the hypercholeretic effect of ursodeoxycholic acid. The aim of the present work was to gain information on this point.
2. Anaesthetized male Wistar rats (∼ 250 g) were used. The animals underwent two-thirds hepatectomy 1, 6 or 12 h before collection of bile samples was begun. Very early after hepatectomy (1 h) spontaneous bile flow and bile acid output were increased. Both returned to values not significantly different from those of the controls at 6 h. Bile flow increased again at the end of the pre-replicative phase. Taurocholate infusion (200 nmol min−1 g−1 calculated liver weight) induced increases in bile flow and bile acid output that were similar in both the control and hepatectomized rats, regardless of the time of the pre-replicative phase considered.
3. Cholic acid and ursodeoxycholic acid were infused (300 nmol min−1 g−1 calculated liver weight) into control and partially hepatectomized rats (at the mid-point of the pre-replicative phase, i.e. 6 h after surgical liver resection). Cholic acid-induced bile flow, bile acid and bicarbonate output expressed per g of remaining liver were similar in control and in hepatectomized rats. By contrast, ursodeoxycholic acid-induced choleresis was profoundly altered during the pre-replicative phase. As expressed per g of remaining liver, bile flow was markedly reduced (− 17%, P &lt; 0.05), in spite of total bile acid output being greatly increased (+ 148%, P &lt; 0.001). The reduced choleretic effect of ursodeoxycholic acid may be due to a lowered stimulation of bicarbonate secretion (− 41%, P &lt; 0.01).
4. Factors known to reduce ursodeoxycholic acid-induced bicarbonate secretion into bile, such as decreased plasma bicarbonate concentrations and lowered total hepatic carbonic anhydrase activity, cannot account for the loss of the ability of ursodeoxycholic acid to stimulate bicarbonate secretion during the pre-replicative phase. However, the bile acid conjugation patterns were dramatically altered early after hepatectomy (6 h). In bile from the control animals the major ursodeoxycholic acid conjugation was with glycine, whereas in hepatectomized rats it was with taurine.
5. In summary, our results indicate that during the prereplicative phase of the regenerating rat liver, a loss occurs in the hypercholeretic effect of bile acids such as ursodeoxycholic acid. However, the choleretic effect of non-hypercholeretic bile acids such as cholic acid and taurocholic acid was not altered. Moreover, the existence of a relationship between the decrease in bile flow and bicarbonate output and the marked increase in the secretion of low-pKa conjugated bile acid derivatives is suggested.
Influence of raising maternal blood pressure with angiotensin II on utero-placental and feto-placental blood velocity indices in the human
Authors: Loquet Ph. , Pipkin F. Broughton , Symonds E. M. , Rubin P. C. 
Published: August 2015

1. The effect of doubling doses of angiotensin II on maternal systemic blood pressure and arcuate and fetal umbilical artery Doppler velocity profiles has been investigated in 10 women in first- and 10 in second-trimester pregnancy. Ten non-pregnant women were also studied.
2. A progressive decrease in the pressor response to angiotensin II in early pregnancy as previously described was confirmed.
3. Angiotensin II induced a significant dose-dependent increase in the pulsatility index (a measure of downstream resistance) in the umbilical artery in both first- and second-trimester patients. There was an apparent increase in the threshold response of the pulsatility index to angiotensin II in the umbilical artery as pregnancy progressed. There was also a significant correlation between changes in maternal systolic or diastolic pressure and change in umbilical artery pulsatility index, but this did not differ between the two trimesters. This suggests that the increase in pulsatility index is related to blood pressure rather than angiotensin II. This is consistent with reports that angiotensin II does not cross the haemo-monochorial placenta.
4. Basal pulsatility index in the arcuate artery fell with increasing gestation. There was a significant inverse association between the evoked change in maternal systemic blood pressure and the change in arcuate artery pulsatility index, suggesting local vasodilatation.
5. We conclude that acutely increasing maternal blood pressure leads to increased vascular resistance on the fetal side of the circulation.
Urinary prostaglandin F2α excretion is not pH-dependent in the conscious rat: implications for the urinary prostaglandin E2/prostaglandin F2α ratio
Authors: Haylor J. , Lote C. J. 
Published: August 2015

1. The influence of urine pH on the urinary excretion of prostaglandin (PG) F2α and the PGE2/PGF2α ratio has been examined in the conscious rat.
2. The basal urinary PGF2α excretion rate of 3.9 pmol/h (n = 23) did not vary with urine pH. In marked contrast, PGE2 excretion increased as the urine became more alkaline. The PGE2/PGF2α ratio therefore progressively increased from 1.5 to 22 as the pH of the urine changed from pH 5.8 to pH 7.8.
3. The independence of PGF2α excretion from urine pH: (a) excludes cyclo-oxygenase as a potential site of action for the pH-dependence of urinary PGE2 excretion; (b) suggests that the urinary PGE2/PGF2α ratio measured in alkaline urine may be a more accurate reflection of the kidneys, ability to synthesize these two prostaglandins in vivo; (c) suggests that control of urine pH is required before the urinary PGE2/PGF2α ratio can be employed as an index of PGE2 9-ketoreductase (EC 1.1.1.189) activity in vivo.
Importance of inspiratory flow rate in the cough response to citric acid inhalation in normal subjects
Authors: Barros Manuel J. , Zammattio Stefano J. , Rees P. John 
Published: August 2015

1. The cough response to inhalation of citric acid is produced mainly by irritation of the larynx and trachea. Variations in the inspiratory flow rate might lead to changes in deposition of the drug, and consequently in the cough threshold.
2. We have studied the effect of three different inspiratory flow rates in 11 normal, non-smoking subjects (nine males, aged 23–39 years), who inhaled nebulized citric acid (2.5–640 mg/l). The test finished when a cough. was produced at each inhalation (cough threshold) or the maximum concentration was reached.
3. The inspiratory flow rate was limited with a fixed resistance and displayed on a screen so that the subjects could reach a constant inspiratory flow rate of 50, 100 and 150 l/min with a submaximal inspiratory effort.
4. The mean (sd) inspiratory flow rates achieved were 51.4 (5.3), 86.2 (16.6) and 134.4 (22.9) l/min. Baseline forced expiratory volume in 1 s and functional vital capacity were not different on the 3 study days.
5. The cough threshold (geometric mean and 95% confidence intervals) was 21 (9–54) mg/l at an inspiratory flow rate of 50 l/min and 43 (13–141) mg/l at 150 l/min (P &lt;0.05). The amount of drug tolerated by the subjects before the cough threshold was achieved was 5.2 (2.0–13.8) mg at an inspiratory flow rate of 50 l/min and 11.6 (3.4–39.8) mg at 150 l/min (P &lt;0.05). The number of coughs per inhalation was 1.6 (1.1–2.0) at an inspiratory flow rate of 50 l/min and 1.1 (0.7–1.5) at 150 l/min (P &lt;0.05).
6. We conclude that lower inspiratory flow rates were associated with a greater cough stimulus in the citric acid challenge procedure used in this study. This may be related to increased laryngeal deposition. The inspiratory flow rate is a variable which should be controlled in the performance of cough challenges with citric acid.
Non-Invasive Assessment of the Cardiovascular Eicosanoids, Thromboxane A2 and Prostacyclin, in Randomly Sampled Males, with Special Reference to the Influence of Inheritance and Environmental Factors
Authors: Wennmalm Å. , Benthin G. , Caidahl K. , Granström E. F. , Lanne B. , Persson L. , Petersson A.-S. , Winell S. 
Published: August 2015

1. We studied, in a random sample of 385 nonsmoking men born in 1968–1969 and 31 men born in 1913 or 1923, whether inheritance and environmental factors influenced platelet activity and vessel wall prostacyclin formation, as reflected non-invasively by the urinary excretion of the 2,3-dinor-metabolites of thromboxane A2 (2,3-dinor-thromboxane B2, Tx-M) and prostacyclin (2,3-dinor-6-keto-prostaglandin F1α, PGI-M), respectively.
2. Fathers of young men with high platelet activity did not excrete more Tx-M than fathers of young men with low platelet activity. Men born in 1913 or 1923 displayed higher Tx-M (563 versus 128 pg/mg of creatinine, P &lt; 0.001) and PGI-M (163 versus 130 pg/mg of creatinine, P &lt; 0.01) excretion than those born in 1968–1969. Excretion of both Tx-M and PGI-M was correlated to the urinary output of noradrenaline and adrenaline.
3. Well-trained subjects did not differ in their excretion of Tx-M or PGI-M from those who did not exercise regularly. A recent acute infection was also unrelated to the excretion of Tx-M or PGI-M. PGI-M excretion was, however, significantly correlated to Tx-M excretion (r = 0.51, P &lt; 0.001).
4. This study provides the first non-invasive evidence that advancing age and sympathoadrenal tone are positively correlated to platelet activity in randomly sampled men, and that paternal inheritance, physical fitness and recent infection lack correlation to platelet activity.
Effect of plasma from patients with essential hypertension on vascular resistance in the isolated perfused rat kidney
Authors: Bachmann Jürgen , Schlüter Hartmut , Storkebaum Walter , Witzel Herbert , Wessels Franz , Zidek Walter 
Published: August 2015

1. Isolated perfused rat kidneys were used to study the effects of plasma fractions obtained by gel filtration from essential hypertensive patients (n = 40) and from normotensive subjects (n = 36) on resistance vessels. Perfusion pressure was recorded at a constant flow.
2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000–1500 Da. The plasma fractions from hypertensive patients used in this study had been shown to increase blood pressure after intravenous injection in rats.
3. In the isolated rat kidneys, the hypertensive fractions increased perfusion pressure by 20 ± 17 mmHg (mean ± SD, range 5–58 mmHg, n = 40). The analogous fractions from normotensive subjects did not change perfusion pressure significantly.
4. In Ca2+-free medium containing 2 mmol/l ethyleneglycol bis-(aminoethyl ether)tetra-acetate, the change in perfusion pressure induced by active plasma fractions was reduced by 95.2 ± 6.3%. Addition of nifedipine to the perfusion medium reduced, but did not abolish, the pressure response of the kidneys.
5. In solutions containing phentolamine or saralasin, vasoconstriction was not reduced.
6. Thus in the active fractions from hypertensive plasma, a vasopressor agent with direct action on resistance vessels can be demonstrated. This substance probably acts by increasing Ca2+ influx in vascular smooth muscle cells.