bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiac metabolism and performance during l-glutamic acid infusion in postoperative cardiac failure
Authors: Pisarenko O. I. , Lepilin M. G. , Ivanov V. E. 
Published: August 2015

1. Intravenous infusion of l-glutamic acid results in the augmentation of the cardiac output and an improvement of the circulation in patients with postoperative cardiac failure. This effect is not accompanied by increased myocardial oxygen demand.
2. Arterial plasma glutamate level rises 10-fold and arterial-coronary sinus plasma glutamate difference increases fivefold during intravenous l-glutamic acid infusion. This leads to cessation of ammonia release from the myocardium, probably due to augmentation of glutamine synthesis and to an increase in alanine formation coupled with a change from lactate release to lactate uptake by the myocardium.
3. The data obtained suggest that the beneficial effect of l-glutamic acid on depressed cardiac function in postoperative patients is related to changes in myocardial metabolism. Glutamic acid may be useful in treatment of circulatory and metabolic disturbances in cardiac failure.
Borderline maintenance of erythrocyte 2,3-diphosphoglycerate concentrations in normoxic type 1 (insulin dependent) diabetic subjects
Authors: Story C. J. , Roberts A. P. , Ryall R. G. 
Published: August 2015

1. Erythrocyte 2,3-diphosphoglycerate and haemoglobin A1C concentrations were measured in 26 clinically normoxic patients with type 1 (insulin dependent) diabetes mellitus. The concentration of 2,3-diphosphoglycerate theoretically required to maintain normal erythrocyte oxygen delivery function in each subject was calculated and compared with the measured concentrations.
2. In the majority of diabetic patients 2,3-diphosphoglycerate concentrations were sufficient to keep the erythrocyte oxygen dissociation curve within the normal range under otherwise normal blood conditions. There was, however, a minority of patients in which this was not true.
3. It is concluded that the increased erythrocyte 2,3-diphosphoglycerate concentrations in clinically normoxic diabetic subjects are generally less than compensatory for the effect of haemoglobin A1C formation on the haemoglobin-oxygen dissociation curve.
Contribution of Vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats
Authors: Hiwatari Masao , Abrahams Josephine M. , Saito Takao , Johnston Colin I. 
Published: August 2015

1. In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increases in blood pressure and left ventricular weight with typical histological changes in the kidney.
2. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 ± 0.5 to 8.9 ± 0.8 pmol/l) but significantly more in SHR (from 5.0 ± 0.6 to 15.8 ±1.2 pmol/l).
3. Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10μg/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 ± 0.9mmHg (P &lt; 0.05) and 9.7 ± 1.7 mmHg (P &lt; 0.05) respectively.
4. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 ± 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats.
5. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggests a close relationship between plasma AVP and severity of hypertension.
6. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.
Vasopressin, aldosterone and renin responses to volume depletion in heart-transplant recipients
Authors: Drieu Luc , Rainfray Muriel , Cabrol Christian , Ardaillou Raymond 
Published: August 2015

1. Plasma arginine vasopressin (AVP), renin activity (PRA) and aldosterone (ALD) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing in 10 untreated healthy subjects (group 1), eight asthmatic patients treated with prednisone (group 2) and 13 heart-transplant recipients treated with prednisone and cyclosporine (group 3). Three different tests for cardiac vagal innervation were performed in the study population. They confirmed that the patients of group 3 were denervated whereas those of groups 1 and 2 had an intact cardiac innervation.
2. Plasma volume depletion after frusemide administration estimated from the rise in plasma proteins was 10–12%. Mean blood pressure was higher in the transplant recipients but did not change in the three groups. Heart rate was also greater in the transplant recipients as a result of vagal denervation. PRA and ALD increased in all the subjects: 2.8, 3.3 and 2.2 times basal value for PRA, 2.7, 4.6 and 2.1 times basal value for ALD in groups 1, 2 and 3 respectively. In contrast, plasma AVP increased only in the two control groups (× 1.45 and × 1.65 in groups 1 and 2 respectively) whereas it was unchanged in the group of heart-transplant recipients (× 1.05).
3. In order to better understand the etiology of the high basal AVP plasma levels observed in group 3, AVP response to a standard water load was studied in eight supplementary heart-transplant recipients: 81.5% of the water load was excreted over 3 h and plasma AVP fell significantly (× 0.76).
4. These results suggest that, in humans, cardiac receptors and innervation play a dominant role in AVP response to volume depletion. In contrast, we found no evidence for a dominant role of cardiac receptors and innervation in mediating renin and aldosterone secretion.
Chemical specificity of coughing in man
Authors: Godden D. J. , Borland C. , Lowry R. , Higenbottam T. W. 
Published: August 2015

1. The purpose of this study was to test whether cough response to inhaled ultrasonically nebulized fluid is dependent on the ionic content of the fluid.
2. Coughing was recorded in human volunteers during inhalation of aqueous solutions in a series of double blind randomized experiments.
3. The occurrence of cough was found to be dependent on the concentration of chloride ions in the inhaled fluid, cough frequency progressively increasing as chloride ion concentration was reduced.
4. It is proposed that the ion composition of the surface lining fluid of the airway may moderate the cough response by means of a chemoreceptor, although tonicity may also be important.
Effect of noradrenaline, vasopressin and angiotensin II on renal prostaglandins in man
Authors: Loup Richard , Favre Laurent , Vallotton Michael B. 
Published: August 2015

1. To examine the response of renal prostaglandins (PG) to systemic and renal vasoconstriction noradrenaline (NA), arginine vasopressin (AVP) and angiotensin II (ANG II) were each infused into eight healthy female subjects for 3 h on different days. Urinary excretion of PGE2, PGF2α and 6-keto-PGF1α was determined hourly.
2. NA and ANG II stimulated excretion of PGF2α significantly, but not of PGE2 or 6-keto-PGF1α AVP stimulated renal PGF2α and 6-keto-PGF1α significantly, but not PGE2.
3. A weak correlation was found between urinary PGF2α and diastolic blood pressure during NA and ANG II infusions, but not during AVP infusion.
4. The release of renal PG does not appear to constitute an obligatory and concomitant response to the blood pressure rise induced by the pressor agonists. The greater response of PGF2α than of PGE2 may result from a preferential direct effect on PGF2α secretion or from an increased conversion of PGE2 into F2α.
The effect of chronic hydrochlorothiazide administration on renal function in the rat
Authors: Walter S. J. , Shirley D. G. 
Published: August 2015

1. Hydrochlorothiazide was administered at two doses to Long-Evans rats for 7–10 days. Both doses resulted in an initial natriuresis and diuresis. After 1 day of treatment the natriuresis abated, but the diuresis persisted.
2. The mechanisms responsible for these chronic effects were investigated by performing clearance and micropuncture studies on all animals; collections were made from late proximal tubules and from early and late regions of distal tubules.
3. Values for total glomerular filtration rate and single-nephron filtration rate in thiazide-treated rats were not significantly different from those in control animals.
4. The delivery of sodium to the end of the proximal convoluted tubule was considerably reduced in each group of thiazide-treated rats. Although sodium delivery to the early distal tubule was also significantly lower than in control animals, the difference had disappeared by the late distal tubule.
5. It is concluded that the return of sodium excretion to control levels during chronic hyrochlorothiazide administration is a consequence of increased fractional reabsorption by the proximal tubules, secondary to a thiazide-induced sodium depletion. This results in less sodium being delivered to the nephron site at which thiazides exert their major inhibitory effect.
6. Fluid delivery to the end of the proximal convoluted tubule and to the early distal tubule was significantly reduced in thiazide-treated rats; in animals given the higher dose of diuretic it was also significantly reduced at the end of the distal tubule. Nevertheless, in both thiazide-treated groups urine flow rate was elevated, suggesting that reabsorption of water from the collecting ducts is reduced during chronic thiazide administration.
Nicotine does not cause ‘bronchitis’ in the rat
Authors: Rogers D. F. , Williams Deborah A. , Jeffery P. K. 
Published: August 2015

1. Nicotine is of interest as a major constituent of cigarette smoke and as an additive to chewing gum used to help patients to stop smoking.
2. Specific pathogen-free rats were given an aerosol or injections of nicotine hydrogen (+) tartrate (l-isomer) for 2 or 3 weeks at three doses and the number of secretory cells in the surface epithelium of airways was determined.
3. By aerosol, a dose giving 10 ng of nicotine/ml of plasma had no effect on secretory cell number.
4. By injection, nicotine had a ‘bi-phasic’ effect depending on dose: it reduced secretory cell number at plasma concentrations of 650 ng/ml of plasma or increased it at 2360 ng/ml of plasma.
5. Thus nicotine alone, given to rats at doses similar to those found in cigarette smokers and those who chew nicotine gum, does not cause secretory cell hyperplasia in the conducting airways of the rat.
A comparison of the relative effectiveness of three transplant preservation fluids upon the integrity and function of rabbit proximal convoluted tubules perfused in vitro
Authors: Pirie Susan C. , Potts D. J. 
Published: August 2015

1. Rabbits were anaesthetized and kidneys removed directly with no flush (group NF), or alternatively kidneys were flushed (group F) with sodium phosphate buffered 140 mmol/1 sucrose (PBsuc 140), Collins C2 (C2) or Euro-Collins (EC) transplant preservation solutions and stored at 4°C for 0–4, 24 or 48 h. Mid-cortical proximal convoluted tubule (PCT) segments were dissected from all groups and set up for microperfusion in vitro. Observations were made of tubule morphology, fluid reabsorption rate (Jv), bath leak of the glomerular marker iothalamate and transmural potential difference (p.d.), both at 37°C and at 15–20°C, in order to compare the relative effectiveness of the solutions in the preservation of tubule integrity and immediate function.
2. Tubules from kidneys flushed with EC and C2 contained luminal debris and frequently had high bath leaks of iothalamate, both indicative of poor preservation of tubule integrity. In contrast, tubules from NF kidneys and PBsuc140-flushed kidneys were free of luminal debris with a lower incidence of high iothalamate leaks.
3. Tubules from PBsuc140-flushed and EC-flushed kidneys after 0–4 and 24 h storage had Jv that were similar to those of NF kidneys. Tubules from all groups of flushed kidneys after 48 h cold storage and all tubules from C2-flushed kidneys showed reduced Jv values. In all cases Jv was reduced to approximately zero when the temperature was lowered to 15–20°C.
4. Transmural p.d. was similar in all groups except for particularly low p.d. values observed in tubules from C2-flushed kidneys after 48 h storage.
5. These observations suggest that PBsuc140 is more effective in the preservation of tubule function during prolonged cold storage than the glucose-based Collins solutions. The marked difference in the effectiveness of C2 and EC contra-indicates the inclusion of magnesium (present in C2) for preservation of kidneys, as judged by experiments on the rabbit.
Effect of angiotensin II on prostanoid synthesis in isolated rat glomeruli
Authors: Podjarny E. , Shapira J. , Rathaus M. , Kariv N. , Bernheim J. 
Published: August 2015

1. The influence of angiotensin II (ANG II) on the synthesis of glomerular prostanoids is controversial, possibly because of the different methodologies employed. In order to assess this inter-relationship isolated rat glomeruli were incubated with and without shaking. The use of shaking during incubation significantly increased the amounts of prostanoid synthesized, most probably because of continuous non-specific activation of phospholipase (PLA2) activity.
2. After preincubation in a non-shaking bath, ANG II was added for a second incubation period. A marked increase of prostaglandin (PG) E2 and, to lesser degree, of thromboxane (TX) B2 was noted, with no change on PGF2α synthesis.
3. These results show (a) that preincubation without shaking, by lowering the non-specific activation of the PLA2 activity, may unmask, in vitro, specific peptide stimulation, and (b) that ANG II, stimulating principally PGE2 synthesis, may modify the vasoactive status of the glomerular vasculature.
Influence of alveolar hypoxia on pulmonary vasomotor responses to almitrine in the dog
Authors: Hughes J. M. B. , Allison D. J. , Goatcher A. , Tripathi A. 
Published: August 2015

1. Almitrine bismesylate (5–10 μg/kg) was given as an intravenous bolus to anaesthetized, paralysed dogs (a) with closed-chest (n = 5) and (b) with open-chest (n = 7) in whom the retrocardiac lobe was separately ventilated. Pulmonary, lobar and systemic haemodynamics were measured under hypoxic, normoxic and hyperoxic conditions. Total pulmonary blood flow was measured by thermodilution and lobar flow by electromagnetic flow meter.
2. In the closed-chest preparations, almitrine caused an increase in pulmonary vascular resistance (PVR) at all levels of inspired oxygen, the increments being 82% (30% O2), 91% (air) and 9% (13% O2). The control PVR varied inversely with arterial Po2 but there was no significant interaction between the almitrine and hypoxia induced vasoconstriction with multiple linear regression analysis.
3. In the open-chest preparations, PVR and lobar vascular resistance (LVR) increased after almitrine by 48% and 41% respectively when both lung and lobe inspired 30% O2. When the lobe was switched to 12.5% O2 or nitrogen (lung inspiring 30%) PVR again increased (+ 52%) after almitrine but LVR decreased in five of seven lobes (lobar flow increasing despite constant cardiac output), the overall change being − 4%. Analysis of covariance showed that the lobar response to almitrine was significantly different under hypoxic conditions compared with hyperoxic (P &lt; 0.05).
4. With ventilation maintained constant, there was no significant change in arterial Po2 after almitrine in any experimental condition.
5. In conclusion, almitrine is generally a pulmonary vasoconstrictor but can dilate vessels when they are constricted by local hypoxia. Almitrine does not enhance local hypoxic vasoconstriction in the dog.
Effects of chronic uraemia on the formation of glucose and urea plus ammonia from l-alanine, l-glutamine and l-serine in isolated rat hepatocytes
Authors: Klim Rita A. , Albajar Marta , Hems Reginald , Williamson Dermot H. 
Published: August 2015

1. The effects of chronic uraemia on glucose production and nitrogen release (urea plus ammonia formation) from alanine, glutamine or serine in isolated rat hepatocytes were studied.
2. Uraemia increased the rate of formation of urea plus ammonia from all three amino acids by 38-93% when they were present at a final concentration of 10 mmol/l. At lower concentrations (2 mmol/l) the rate of nitrogen release was not significantly increased.
3. Hepatocytes from normal rats whose food intake had been restricted to the level of that of uraemic rats did not show the increased rates of nitrogen release.
4. The increased rates of nitrogen release with hepatocytes from uraemic rats were not accompanied by increased rates of glucose synthesis. Instead, accumulation of metabolic intermediates occurred: lactate and pyruvate (alanine or serine as substrates) and glutamate (glutamine as substrate).
5. Livers of uraemic rats had increased activities of glutarninase (30%) and serine dehydratase (100%).
6. Hepatocytes from normal rats treated with phlorhizin to increase the plasma glucagon/insulin ratio behaved in a similar manner to hepatocytes from uraemic rats. They had increased serine dehydratase activity, and increased rates of utilization of serine or glutamine.
7. The possible implications of these findings for human uraemia are discussed.
Ventilatory sensitivity to inhaled carbon dioxide around the control point during exercise
Authors: Cummin Andrew R. C. , Alison Jennifer , Jacobi Margaret S. , Iyawe Vincent I. , Saunders Kenneth B. 
Published: August 2015

1. Rapid steady-state CO2 responses were determined in five normal adults at rest and at up to six levels of exercise by injecting pure CO2 at a constant flow into the inspiratory limb of a breathing circuit.
2. Ventilation (V) was measured with a dry gas meter and Pco2 at the mouth was recorded by a mass spectrometer. Mean alveolar Pco2 (Paco2) was taken as equal to end-tidal Pco2 at rest, and during exercise was derived graphically from the sloping alveolar plateaus. The accuracy of the latter method was checked in separate experiments against arterial Pco2 (Paco2).
3. The mean results showed a linear relationship between change in Paco2 and change in V for work loads ranging from rest to 75 W (r = 0.94–0.98). Above 75 W the response became concave down with an initial essentially isocapnic phase.
4. This suggests that during exercise there is a large increase in CO2 sensitivity about the control point.
Evidence for adaptive diet-induced thermogenesis in man during intravenous nutrition with hypertonic glucose
Authors: King R. F. G. J. , McMahon M. J. , Almond D. J. 
Published: August 2015

1. This study was designed to investigate the thermogenic effect of intravenously administered nutrition with glucose (given with a fixed nitrogen intake of 12.5 g daily as amino acids) as the principal source of energy. The protocol was designed so that each patient received their energy intake in five consecutive periods of 3 days with intakes ranging from 6650 to 17100 kJ/day with increments or decrements of 2600 kJ.
2. Thermogenesis from administered glucose was evident between levels of energy supply of 6650 kJ/day and 17100 kJ/day. The progressive rise in oxygen consumption and carbon dioxide production accounted for a total of 31% of the additional glucose which was administered. The net rate of fat synthesis from glucose reached a maximum 147 g/day at an energy supply of 14 500 kJ/day.
3. This study suggests that both fat synthesis and the associated obligatory thermogenesis is the main component of diet-induced thermogenesis in response to glucose intakes in excess of 150 kJ day−1 kg−1. If the energy cost of fat synthesis (fat associated obligatory thermogenesis) is taken to be 22% of the total energy of the increase in glucose supplied, then only 9% (31–22%) of the glucose can be accounted for by adaptive thermogenesis.
Binding of glycosaminoglycans to sodium urate and uric acid crystals
Authors: Fellström Bengt , Lindsjö Monica , Danielson Bo G. , Ljunghall Sverker , Wikström Björn 
Published: August 2015

1. The binding of heparin, chondroitin sulphate and the low molecular weight heparin analogue pentosan polysulphate to sodium urate and uric acid crystals was studied by the use of competitive binding technique. Trace amounts of radioactively labelled glycosaminoglycans were used in the binding step, and varying amounts of unlabelled glycosaminoglycans for the competition experiments.
2. The experiments were carried out in 140 mmol/l NaCl at pH 6, with or without 5 mmol/l CaCl2 in the solution.
3. A reversible and almost complete binding of heparin and chondroitin sulphate to sodium urate crystals did occur in the presence of calcium, whereas pentosan polysulphate bound incompletely. The binding was much less pronounced in the calcium-free conditions.
4. Uric acid crystals did not bind any of the three inhibitors, not even with calcium present.
5. The clinical relevance depends on whether sodium urate microcrystals are present in the urine of calcium stone patients, to cause a binding and thereby a masking or inactivation of these inhibitors in the urine, which seems to be possible in the presence of calcium. However, the potential of pentosan polysulphate for the treatment of calcium stone patients does not seem to be at risk from this effect.
Renal water excretion before and after remission of nephrotic syndrome: Relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading
Authors: Pedersen E. B. , Danielsen H. , Sørensen S. S. , Jespersen B. 
Published: August 2015

1. An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (Cwater), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading.
2. D and Cwater increased to a significantly lower level (P &lt; 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and Cwater were normal after remission of the syndrome. The maximum increase in Cwater (ΔCwater max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group.
3. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P &lt; 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group.
4. The elevation in ΔCwatermax after remission was accompanied by an increase in Ccr in all patients and ΔCwatermax. and Ccr were significantly correlated (ρ = 0.600, n = 16, P &lt; 0.05). No relationship was found between the change in ΔCwater max. and ANG II and Aldo.
5. AVP was significantly suppressed in patients with nephrotic syndrome before remission, but not after remission nor in control subjects, so that although AVP did not differ in nephrotic patients before and after remission, AVP cannot be excluded as a contributory factor to the reduction in Cwater in the nephrotic syndrome.
6. It is concluded that patients with nephrotic syndrome excrete an oral water load slower than control subjects and that the excretion rate is normal after remission of the syndrome. It is suggested that the normalization of Cwater may be attributed to an increase in glomerular filtration rate or a decrease in proximal tubular sodium reabsorption, although a possible role for AVP has not been excluded.