bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical and Electrophysiological Studies of Peripheral Nerve Function in Patients with Chronic Liver Disease
Authors: Morgan M. H. , Read A. E. , Campbell M. J. 
Published: August 2015

1. A series of 24 (eight alcoholic, 16 non-alcoholic) patients with histologically confirmed cirrhosis of the liver was examined for clinical and electrodiagnostic evidence of peripheral nerve damage.
2. Clinical evidence of mild, asymptomatic peripheral neuropathy was found in only three (19%) of the non-alcoholic group.
3. Electrodiagnostic tests on the median, ulnar, lateral popliteal and sural nerves were undertaken for each patient. Abnormalities of distal motor latency, motor conduction velocity or sensory action potential amplitudes were noted in 17 (71%). Exclusion of three patients in whom abnormality was confined to the median nerve, with the possibility of carpal tunnel compression, gave a final overall figure of 14 (58%). In the non-alcoholic group there were ten (63%) with abnormalities.
4. Sensory action potential amplitudes were reduced in 16 (67%), but only eight (33%) had abnormal distal motor latencies or motor conduction velocities. Nerves were affected in a patchy and unpredictable manner.
5. The number of abnormal electrodiagnostic tests for each patient bore no direct relation to the length of history, nor to the severity of liver damage.
6. In a selected group of patients with no other demonstrable cause of peripheral nerve damage, there was a positive correlation between the number of abnormal electrodiagnostic tests and the degree of slowing of the EEG mean dominant frequency. Possible implications of this finding are discussed.
Antihypertensive Effect of Prolonged Blockade of Angiotensin Formation in Benign and Malignant, one- and two-Kidney Goldblatt Hypertensive Rats
Authors: Bengis R. G. , Coleman T. G. 
Published: August 2015

1. The effect of chronic inhibition of angiotensin II formation was investigated in four groups of hypertensive rats. Benign hypertension was produced by placing a 0·25 mm-diameter silver clip on the renal artery; a 0·20 mm clip was used to create malignant hypertension. A two-kidney model had a clip plus intact contralateral kidney and a one-kidney model had a clip plus contralateral nephrectomy. Benign and malignant groups were prepared in both the one-kidney and two-kidney variations. Converting enzyme inhibitor (SQ 14.225) was given to these four groups for 1 week in drinking water and average intake ranged from 33 to 77 mg/day.
2. The two malignant groups had the highest plasma renin activities and they showed a precipitous fall in arterial pressure in the first 24 h of inhibition of angiotensin formation. All groups showed an additional slow decline in pressure during the remaining 6 days of inhibition. Changes in heart rate and sodium excretion were variable but, in general, heart rate decreased during inhibition.
3. Arterial pressure did not become normal with inhibition in either of the one-kidney models: decreases to 126 and 132 mmHg were observed in the benign and malignant groups respectively. Three of the malignant one-kidney animals became uraemic with inhibition and one died before inhibition was discontinued.
4. Arterial pressure was reduced to normal pressure (95 mmHg) after 1 week of inhibition in both the benign and malignant two-kidney models.
5. It appears that normal pressure was restored in the two-kidney model but not in the one-kidney model because of the presence of the intact contralateral kidney. The physiological basis for this difference is not known but changes in renal excretory function may be involved.
An 8 Month Longitudinal Study of Changes in Elastic and Muscular Arteries and Veins of the Rabbit with Sustained Hypertension after Abdominal Aorta Constriction
Authors: Bevan R. D. , Eggena P. , Hume W. R. , Lais L. T. , Van Marthens E. , Bevan J. A. 
Published: August 2015

1. Long-term changes in the function and structure of arteries and veins in response to an elevation in arterial pressure have been studied in the rabbit after partial abdominal aorta constriction.
2. Transient changes occur in the vasculature in association with the rise in arterial pressure.
3. The dominant change seen after arterial pressure elevation has been maintained for 8 months is an increase in arterial wall mass, including an increase in vascular smooth muscle cell number, and in some arteries an increase in internal diameter.
4. It may be inferred from this limited study of elastic and muscular arteries that structural alteration represents the over-riding response of the vasculature to an elevation in intramural pressure.
The Composition of Low-Density Lipoprotein and Very-Low-Density Lipoprotein Subfractions in Primary Hypothyroidism and the Effect of Hormone-Replacement Therapy
Authors: Ballantyne Fiona C. , Epenetos A. A. , Caslake Muriel , Forsythe S. , Ballantyne D. 
Published: August 2015

1. The lipid and protein composition of subfractions of plasma low-density lipoprotein (LDL) has been determined in nine patients with primary hypothyroidism before and after 3 months of thyroxine therapy. Analyses were also made of subfractions of very-low-density lipoprotein (VLDL) in four of the patients.
2. Before therapy seven of the patients had elevated LDL-cholesterol and two had increased VLDL-cholesterol concentrations. On thyroxine replacement the mean LDL-cholesterol fell to normal. No significant change occurred in the concentration of cholesterol in VLDL or in high-density lipoprotein (HDL).
3. The concentrations of cholesterol, triglyceride and apolipoprotein B (apoB) were increased in the LDL subfraction of Sf 10·4–20, which corresponds mainly to intermediate-density lipoprotein. This subfraction showed a marked fall on therapy. The cholesterol and apoB concentrations in the major LDL fraction of Sf 5·7–12 also decreased on therapy, but the fall in the subfraction of Sf 3·5–6·5 did not reach statistical significance.
4. Only the VLDL subfraction of smallest size (Sf 20–60) had any abnormality before therapy, with an increased concentration of cholesterol. On thyroxine the concentration of triglyceride rose in the VLDL subfractions.
5. These data suggest that thyroxine exerts its major effect on lipoprotein metabolism by promoting the conversion into LDL of intermediate-density lipoprotein, formed by catabolism of VLDL.
Effect of 1 Year's Therapy in Essential Hypertension on Systemic Haemodynamics Studied before and after ‘Total’ Autonomic Blockade
Authors: Jennings G. L. , Korner P. I. , Esler M. D. 
Published: August 2015

1. The haemodynamics of ten patients with essential hypertension were studied before treatment (study 1) and again 1 week after cessation of 1 year's antihypertensive drug therapy (study 2). On each occasion measurements of mean arterial pressure (MAP), cardiac index (CI) and total peripheral resistance index (TPRI) were made before and after ‘total’ pharmacological autonomic blockade (with intravenous propranolol, atropine, phentolamine and clonidine); measurements after ‘total’ autonomic blockade were used to assess the magnitude of the ‘non-autonomic’ component of TPRI, which reflects humoral or structural alterations in the vasculature.
2. The findings before ‘total’ autonomic blockade during study 2 showed that MAP was 18 ± 8 mmHg below the value (135 mmHg) observed during study 1 before treatment, and TPRI had fallen by 33% (P &lt; 0·05) and CI had increased by 23% (P &lt; 0·05).
3. After ‘total’ autonomic blockade the differences in the ‘non-autonomic’ components of the different variables were similar, with ‘non-autonomic’ MAP 14 ± 4 mmHg lower in study 2, TPRI 42% lower (P &lt; 0·005) and CI 28% higher. The value in ‘non-autonomic’ TPRI was now the same as values previously observed in normotensive subjects.
4. We conclude that after 1 year's successful treatment there is complete restoration of ‘non-autonomic’ TPRI as a secondary consequence of the blood pressure reduction.
Dependence of Deoxycorticosterone/Salt Hypertension in the Rat on the Activity of Adrenergic Cardiac Nerves
Authors: Bell C. , McLachlan Elspeth M. 
Published: August 2015

1. Chronic hypertension was induced in Wistar rats with intact kidneys by subcutaneous implantation of 50 mg of deoxycorticosterone acetate (DOC A) in wax and addition of sodium chloride (9 g/l) to the drinking water.
2. The development of DOCA/salt hypertension, as monitored by tail-cuff plethysmography, was prevented by: (a) destruction of the peripheral adrenergic nerves with neonatal administration of guanethidine (80 mg/kg subcutaneously for the first 14 days postnatally); (b) bilateral stellate ganglionectomy; (c) oral administration of the β-adrenoreceptor antagonists propranolol or atenolol (1 mg day−1 kg−1) during the period of DOCA/salt treatment.
3. The dose of DOCA used was sufficient to inhibit the atrial Uptake2 pathway completely: this process appears to participate in termination of action of neurally released noradrenaline in the heart.
4. It is suggested that this model of DOCA/salt hypertension is due to adrenergic enhancement of cardiac output in the presence of an increased sodium load. The enhancement may be partly due to deficient myocardial inactivation of noradrenaline.
Comparison of 15N-Labelled Glycine, Aspartate, Valine and Leucine for Measurement of Whole-Body Protein Turnover
Authors: Taruvinga M. , Jackson A. A. , Golden M. H. N. 
Published: August 2015

1. Whole-body protein turnover was measured in rats by constant infusion of 15N-labelled glycine, aspartate, valine and leucine and measuring the enrichment of hepatic and renal urea and ammonia nitrogen.
2. The values obtained with [15N]glycine were comparable with values reported with methods based on different assumptions.
3. [15N]Aspartate gave rise to an increased enrichment of urea and ammonia and hence to lower protein-turnover rates.
4. [15N]Valine and [15N]leucine gave low enrichments of nitrogenous end products and hence to high protein-turnover rates.
5. All 15N-labelled amino acids are not equally suitable for measuring whole-body protein turnover by the end-product method. The relative amounts of 15N going to the end products can be predicted from the known individual metabolism of aspartate and the branched-chain amino acids.
The Adenylate Cyclase System in Human Liver: Characterization, Subcellular Distribution and Hormonal Sensitivity in Normal or Cirrhotic Adult, and in Foetal Liver
Authors: Pecker F. , Duvaldestin P. , Berthelot P. , Hanoune J. 
Published: August 2015

1. Adenylate cyclase (EC 4.6.1.1) activity was characterized in human liver, and its subcellular distribution compared with that of three other potential enzyme markers of the pericellular membrane: leucine aminopeptidase (EC 3.4.11.1), γ-glutamyltransferase (EC 2.3.2.2) and 5′-nucleotidase (EC 3.1.3.5). Although these three enzyme activities were detected in each of the subcellular fractions studied, 85% of the total adenylate cyclase activity was found in the 1000 g pellet (‘nuclear’ fraction) with a threefold increase in specific activity as compared with the homogenate. No adenylate cyclase activity existed in the 150 000 g supernatant fraction.
2. In the ‘nuclear’ fraction, adenylate cyclase activity was increased in a dose-dependent fashion by glucagon with a half-maximal stimulation at 10 nmol/l and a maximal four- to seven-fold increase at 1 μmol/l. Catecholamines activated adenylate cyclase 2·5- to three-fold, with an order of potency (protokylol &gt; isoprenaline &gt; adrenaline &gt; noradrenaline) typical of a β2-adrenoreceptor. Prostaglandin E1 and NaF also stimulated cyclase two- and four-fold respectively. Insulin, serotonin, dopamine, thyroid-stimulating hormone and ACTH had no effect. Adenosine provoked a weak inhibition at 0·1 mmol/l. Finally guanosine triphosphate and 5′-guanylyl imidodiphosphate induced a marked increase in basal activity, four- and eight-fold respectively, but both reduced the relative increase in enzyme activity due to glucagon or adrenaline.
3. Cyclase from foetal liver (12–16 weeks old) and cirrhotic adult liver appeared to behave similarly to that from normal liver; however, foetal cyclase was more active, and cirrhotic enzyme less active than normal adult liver. Both systems responded to catecholamines via a β2-adrenoreceptor.
4. These results validate the use of rat liver adenylate cyclase as a tool for pharmacological and physiological studies.
Effect of Isoprenaline on the Plasma Concentrations of Angiotensin III in Rats
Authors: Meyer D. K. , Eisenreich M. , Nutto D. 
Published: August 2015

1. A new column-chromatographic method is described for the simple and reproducible determination of the concentration of [des-Asp1] angiotensin II (angiotensin III) in rat plasma.
2. The method uses the different abilities of the ion-exchange resins Dowex 1 (X8) and Bio Rex 70 to bind angiotensin II and angiotensin III. Under the conditions used, Bio Rex 70 binds only angiotensin III. Angiotensin II and its hexapeptide metabolite [des-Asp1,des-Arg2]angiotensin II pass the resin with the effluent. Dowex 1 (X8) binds angiotensin II and the hexapeptide metabolite, whereas it does not extract angiotensin III. It does not separate angiotensin II from the hexapeptide. Therefore the sum of both peptides is expressed as angiotensin II-like activity. The ratio of the concentrations, angiotensin II/hexapeptide, was 5:1.
3. In normal rats the plasma concentration of angiotensin III was 20 fmol/ml (sd 15; n = 8), and angiotensin II-like activity was 60 fmol/ml (sd 35; n = 8).
4. The β-sympathomimetic amine isoprenaline caused a time- and dose-dependent increase in plasma angiotensin III and angiotensin II-like activities.
5. Under the conditions studied angiotensin III contributed approximately 25% to the total amount of angiotensins in plasma.
Dissociation in the Excretion of Different Aldosterone Metabolites and Unmetabolized (‘Free’) Aldosterone in Hypertension
Authors: Abdelhamid S. , Vecsei P. , Haack D. , Gless K.-H. , Walb D. , Lichtwald K. , Fiegel P. 
Published: August 2015

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12·3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B).
2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected.
3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.
Effect of Ouabain in Therapeutic Concentrations on K+ Exchange and Contraction of Human and Rabbit Myocardium
Authors: Poole-Wilson P. A. , Galindez E. , Fry C. H. 
Published: August 2015

1. Experiments were undertaken on strips of human atrial and ventricular muscle, on right ventricular rabbit papillary muscles and on the rabbit interventricular septum.
2. In all preparations an increase of developed tension after 30 min exposure to ouabain was apparent only at or above a concentration of 10−7 mol/l (73 μg/l).
3. In the rabbit septum there was a net loss of potassium on exposure to ouabain if the concentration was greater than 10−7 mol/l. There was no net loss, or gain, of potassium at lower concentrations. Loss of potassium, indicating inhibition of the sodium pump, could not be dissociated from the positive inotropic effect of ouabain.
4. The greater sensitivity to ouabain of human myocardium in vivo (10−8 mol/l) than in vitro (10−7 mol/l) may be due to cellular changes occurring in isolated preparations.
Are Mineralocorticoid Receptors Present in Human Renal Adenocarcinoma?
Authors: Rafestin-Oblin M. E. , Roth-Meyer C. , Claire M. , Michaud A. , Baviera E. , Brisset J. M. , Corvol P. 
Published: August 2015

1. The presence of high-affinity sites for [3H]-aldosterone was shown in the normal human renal tissue.
2. [3H]Aldosterone and [3H]dexamethasone binding were studied in human renal adenocarcinoma and in uninvolved external cortex, in 22 patients undergoing nephrectomy for renal adenocarcinoma. Tissue incubations were performed with either [3H]aldosterone (5 × 10−10 mol/l; 5 × 10−9 mol/l in the presence of unlabelled glucocorticoids) or [3H]dexamethasone (5 × 10−9 mol/l).
3. Cytosol [3H]aldosterone binding was six- to seven-fold lower (P &lt; 0·001) in neoplastic than normal tissue. [3H]Dexamethasone binding was about twofold higher in neoplastic than in normal tissue. This difference was not significant.
4. Nuclear uptake experiments showed that, both in cytosol fractions and nuclei, [3H]aldosterone binding was lower in adenocarcinoma than in normal cortex.
5. The very low binding of [3H] aldosterone suggests that mineralocorticoid receptors are absent in renal adenocarcinoma, an hypothesis in line with the proximal origin of these tumours.
Distribution of Circulating Immunoreactive Components of Parathyroid Hormone in Normal Subjects and in Patients with Primary and Secondary Hyperparathyroidism: The Role of the Kidney and of the Serum Calcium Concentration
Authors: Dambacher M. A. , Fischer J. A. , Hunziker W. H. , Born W. , Moran J. , Roth H.-R. , Delvin E. E. , Glorieux F. H. 
Published: August 2015

1. The distribution of intact parathyroid hormone-(1–84) [PTH-(1–84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1–84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000–7000 (peak II) and immunoreactive components co-eluting with human PTH-(1–12) (peak III) were observed.
2. Mean concentrations of intact PTH-(1–84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1–84).
3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1–84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.
Effect of Age on Noradrenaline Sensitivity of Mesenteric Resistance Vessels in Spontaneously Hypertensive and Wistar—Kyoto Rats
Authors: Mulvany M. J. , Aalkjær C. , Christensen J. 
Published: August 2015

1. We have compared the noradrenaline sensitivity of 150 μm arterial resistance vessels taken from a specific place in the mesenteric bed of spontaneously hypertensive (SH) rats and of control Wistar—Kyoto (WK) rats at three ages: 6 weeks, 12 weeks and 24 weeks.
2. The noradrenaline sensitivity of the vessels under normal conditions was the same at all ages in both SH and WK rats (ED50 about 3 μmol/l).
3. After addition of cocaine (which inhibits the uptake of noradrenaline in the nerve terminals) all vessels became more sensitive to noradrenaline, but at all ages the increase in sensitivity was greater in the vessels of SH rats, suggesting that the smooth muscle cells in these vessels had a greater intrinsic noradrenaline sensitivity than the vessels of WK rats.
4. Since elevation of the blood pressure in the SH rats occurs mainly between the ages of 6 and 12 weeks, the results suggest that the greater intrinsic smooth muscle cell sensitivity of the SH rat vessels is a factor which is amongst the primary factors responsible for the development of hypertension in the SH rat.
Pressor Responsiveness to Angiotensin in Renovascular and Steroid Hypertension
Authors: Marks E. S. , Thurston H. , Bing R. F. , Swales J. D. 
Published: August 2015

1. The pressor response to angiotensin II was reduced in rats with early (&lt;6 weeks) and chronic (&gt;4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA—salt hypertension.
2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness.
3. After bilateral nephrectomy the pressor responses to angiotensin were similar.
4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.
Radiolabelled Bile Acid Clearance in Control Subjects and Patients with Liver Disease
Authors: Engelking L. R. , Barnes S. , Dasher C. A. , Naftel D. C. , Hirschowitz B. I. 
Published: August 2015

1. The serum bile acid disappearances of tracer doses of [24-14C]cholic acid and [1-14C]-glycocholic acid were studied in eight normal subjects and 11 patients with chronic liver disease (with or without cholestasis) in order to determine the effect of liver disease on hepatic clearances, reflux of conjugated cholic acid and initial distribution volume of each tracer.
2. Total cholic acid clearance was significantly reduced from normal (7·2 ± 0·7 ml min−1 kg−1, mean ± se) in patients with liver disease (69–88%, group means) as were unconjugated cholic acid (51–68%) and glycocholic acid (66–83%) clearance.
3. Extensive regurgitation of labelled conjugated cholic acid (after unconjugated cholic acid tracer injection) among cholestatic patients accounted for 69 ± 5% of total 14C remaining in serum at 70 min, thus masking a less-impaired uptake process.
4. The hepatic extraction efficiency for conjugated cholic acid among controls (86 ± 8%) was greater than that for unconjugated cholic acid (60 ± 4%), and was greatly reduced among patients (7–27%, group means).
5. Normal subjects and patients with cirrhosis without cholestasis did not distribute the isotope to extravascular, extrahepatic spaces, in contrast to cholestatic patients with serum bile acid concentration &gt; 149μmol/l.
6. Careful evaluation of serum disappearance of bile acids as well as chromatographic separation of regurgitated metabolites, could provide investigators with indirect evidence of defects in the rate-limiting steps (uptake, conjugation or excretion) of hepatic bile acid transport.