bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reduced oxygen consumption induced by vasopressin in dogs depends on systemic administration
Authors: Liard Jean-Francois 
Published: August 2015

1. Arginine vasopressin reduces whole-body oxygen consumption in conscious dogs. To determine whether this decrease could result from limited oxygen delivery, studies were performed in two groups of chronically instrumented dogs.
2. In the first group (n = 7), vasopressin was infused at a rate of 18.5 pmol min−1 kg−1 while the animals were breathing 10% oxygen. Hypoxaemia alone (arterial partial pressure of oxygen 4.67 kPa) decreased whole-body oxygen delivery by 30%. The fall in whole-body oxygen consumption induced by vasopressin during hypoxaemia was not different from that measured under normoxic conditions, even though whole-body oxygen delivery was more reduced.
3. In a second group of seven dogs, hindquarter blood flow (electromagnetic flowmeter on lower abdominal aorta) and oxygen consumption (blood flow multiplied by arteriovenous oxygen difference) were measured as infusions of vasopressin were given either systemically or into the lower abdominal aorta. Systemic vasopressin infusions at 0.92, 4.6 and 18.5 pmol min−1 kg−1 reduced hindquarter blood flow, oxygen delivery and oxygen consumption, but the decreases in blood flow and oxygen delivery were dose-related whereas that in oxygen consumption was not. Intra-arterial infusions of vasopressin that increased venous concentrations as much as or more than systemic infusion of 0.92 pmol of vasopressin min−1 kg−1 had no effect on oxygen consumption, even though the higher intra-arterial rate reduced blood flow and oxygen delivery as much as the systemic infusion. Thus systemic but not locally administered vasopressin reduced hindquarter oxygen consumption.
4. Small to moderate mechanically induced reductions in hindquarter blood flow resulted in a smaller decrease in oxygen consumption than equivalent blood flow reductions induced by vasopressin. On the contrary, large mechanically induced flow reductions resulted in a larger decrease in oxygen consumption than those induced by vasopressin.
5. These results suggest that the decrease in hindquarter oxygen consumption induced by systemic vasopressin administration cannot be primarily a consequence of oxygen delivery limitation.
Plasma and platelet free catecholamine concentrations in patients with familial hypercholesterolaemia
Authors: Smith C. C. T. , Prichard B. N. C. , Betteridge D. J. 
Published: August 2015

1. Plasma and platelet free catecholamine concentrations were measured in 22 normal subjects and in 10 treated and 11 untreated patients with heterozygous familial hypercholesterolaemia.
2. Plasma noradrenaline concentrations were significantly higher in both treated and untreated hypercholesterolaemic patients than in normal subjects. Adrenaline concentrations did not differ.
3. Platelet noradrenaline levels were higher in untreated hypercholesterolaemic patients than in normal subjects.
4. Positive correlations between the plasma noradrenaline concentration and the platelet noradrenaline concentration were observed in both normal subjects and hypercholesterolaemic patients.
5. Combining the data for normal subjects and hypercholesterolaemic patients revealed that the plasma noradrenaline concentration correlated positively with the plasma cholesterol concentration. The platelet noradrenaline concentration was also found to correlate with the plasma cholesterol concentration.
6. Our results suggest that an increased plasma cholesterol concentration may be associated with increased sympathetic nervous system activity as indicated by elevated plasma and platelet noradrenaline levels. Increases in circulating catecholamines may contribute to the platelet hyperaggregability seen in familial hypercholesterolaemia.
Coronary haemodynamic effects of angiotensin II in mild essential hypertension in man
Authors: Magrini Fabio , Reggiani Paolo , Ciulla Michele , Meazza Roberto , Fratianni Gerardina 
Published: August 2015

1. The present investigation was carried out to elucidate the possible role of the renin-angiotensin system in modulating coronary vasomotor responses in eight patients with uncomplicated mild essential hypertension with no electrocardiographic-echocardiographic evidence of left ventricular hypertrophy.
2. Systemic and coronary haemodynamics were monitored at baseline and during intravenous infusion of angiotensin II at a subpressor dose (3 ng min−1 kg−1 for 15 min) and at a pressor dose (13 ng min−1 kg−1 for 15 min) both at rest and during handgrip exercise. Infusion of the subpressor dose of angiotensin II decreased coronary sinus blood flow at rest (207 ± 10 versus 182 ± 9 ml/min, P &lt; 0.05) without a significant change in mean arterial pressure, heart rate or mean right atrial pressure. The performance of handgrip at baseline and during infusion of the subpressor dose of angiotensin II resulted in 55% (321 ± 13 versus 207 ± 10 ml/min) and 44% (263 ± 16 versus 182 ± 9 ml/min) increases in coronary sinus blood flow, respectively, in response to comparable increments in the rate-pressure product. At rest, infusion of the pressor dose of angiotensin II increased both coronary sinus blood flow (235 ± 11 versus 207 ± 10 ml/min, P&lt;0.01) and the rate-pressure product (134 ± 5 versus 111 ± 8 mmHg beats/min, P&lt;0.01). The increase in coronary sinus blood flow during isometric exercise was less than control (309 ± 18 versus 321 ± 13 ml/min, P&lt;0.01).
3. It is thus concluded that (1) the opposite effects of angiotensin II on coronary blood flow are dose-dependent, and that (2) angiotensin II competes with the ability of the coronary arteries to dilate during handgrip exercise.
Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs
Authors: Kaczmarczyk Gabriele , Schröder Klaus , Lampe Dirk , Mohnhaupt Rainer 
Published: August 2015

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homoeostatic responses to an acute extracellular fluid volume expansion.
2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day−1 kg−1 body weight).
3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min−1 kg−1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 ± 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments).
4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 ± 0.3 ml min−1 kg−1 body weight, mean ± sem) increased by 1 ml min−1 kg−1.
5. Plasma renin activity [control 0.85 ± 0.15 (RAP-f) and 1.08 ± 0.23 (RAP-sc) pmol of angiotensin I h−1 ml−1] decreased similarly in both protocols.
6. Renal sodium excretion, fractional sodium excretion and urine volume increased more in the RAP-f experiments than in the RAP-sc experiments (P&lt;0.05), renal sodium excretion from 8.2 to 70.1 (RAP-f) and from 7.7 to 47.4 (RAP-sc) μmol min−1 kg−1 body weight, fractional sodium excretion from 1.1 to 8.0 (RAP-f) and from 1.0 to 5.4 (RAP-sc)% and urine volume from 39 to 586 (RAP-f) and from 38 to 471 (RAP-sc) μl min−1 kg−1 body weight.
7. In the RAP-f experiments as well as in the RAP-sc experiments, urinary sodium excretion increased with expansion of the extracellular fluid volume, which increased by a maximum of 21% (fasting extracellular fluid volume: 206 ± 4 ml/kg body weight, six dogs, 28 days).
8. The increase in renal arterial pressure contributed significantly to the renal homoeostatic response, as 21% less urine and 31% less sodium were excreted when the extracellular fluid volume was expanded and the renal arterial pressure was kept constant below control pressure rather than being allowed to rise. The differences in sodium and water excretion were mainly due to the effect of renal arterial pressure on tubular reabsorption. However, the striking increase in sodium and urine excretion which occurred despite the reduction in renal arterial pressure emphasizes the importance of other homoeostatic factors involved in body fluid regulation.
Exposure of rat colonic mucosa to human semen in vivo induces mucosal cytolysis, abolishes fluid absorption and raises paracellular permeability
Authors: Mendizabal M. V. , Naftalin R. J. 
Published: August 2015

1. The effects of human semen on rat descending colon fluid absorption, permeability to 3H-labelled polyethylene glycol 4000 and the histological appearance of the mucosa were examined. Also, the semen was fractioned by centrifugation into plasma and sperm fractions and the effects of these fractions on rat colonic function were examined. The effects of trypsin and bacterial collagenase, mimetics of acrosin and seminal collagenase activity, were examined in order to investigate which component of human semen alters colonic permeability.
2. Contact between human semen and rat descending colonic mucosa for 3 h decreased fluid absorption from 52.0 ± 2.9 μl h−1 cm−2 (control) to 10.7 ± 3.4 μl h−1 cm−2 (P &gt;0.001), increased the permeability to polyethylene glycol 4000 from 0.099 ± 0.006 cm/h (control) to 0.31 ± 0.04 cm/h (P&gt;0.001) and caused cytolysis of the surface mucosa.
3. Spermatazoa inside the colonic lumen were destroyed within 1 h with release of acrosomal contents; this raised the activity of the acrosomal proteolytic enzyme acrosin by 40-fold (P &gt;0.005) and of seminal plasma metalloproteinase (collagenase) by about twofold (mean activity 1623 ± 240 units/ml of luminal fluid).
4. The changes in colonic permeability induced by seminal plasma were similar to those induced by similar activities of clostridial collagenase.
5. We conclude that seminal collagenase is present in sufficient amounts to cause acute damage to the colonic mucosa, and that this could be a factor in facilitating viral transmission across the colonic wall.
A novel mucin sulphatase from human faeces: its identification, purification and characterization
Authors: Tsai H. H. , Sunderland D. , Gibson G. R. , Hart C. A. , Rhodes J. M. 
Published: August 2015

1. Colonic mucus is heavily sulphated and it is likely that this contributes considerably to its resistance to degradation by bacterial enzymes. The presence of a mucin-desulphating enzyme in faeces could therefore be very important in determining the rate of degradation of secreted mucus and hence the level of protection of the mucosa.
2. A novel assay for mucin sulphatase has been developed using biologically labelled human colonic [35S]sulphomucin as a substrate and a mucin sulphatase has been purified from faeces by sequential high-performance gel filtration and ion-exchange chromatography.
3. The mucin sulphatase has been shown to have a pH optimum of 4.5 and activity over the pH range 3–7. It has a pI of 4.0 and is inhibited by inorganic sulphate and phosphate. The purified enzyme preparation gave a single band on electrophoresis with a molecular mass of 15000 Da. It has a Km of 41.9 mmol/l and a Vmax. of 1.17 katal/ kg for glucose 6-sulphate. The enzyme was also shown to enhance fivefold the deglycosylation of [3H]glucosamine-labelled mucin by a faecal mucin glycosidase preparation.
4. Two bacteroides spp. isolated from normal human faeces, Bacteroides fragilis and B. thetaiotaomicron, were found to be producers of mucin-desulphating enzymes.
5. Mucin sulphatase is likely to be critical in determining the rate of enzymic degradation of secreted colonic mucin.
Proton efflux from rat skeletal muscle in vivo: changes in hypertension
Authors: Kemp G. J. , Thompson C. H. , Radda G. K. 
Published: August 2015

1. An analysis of the recovery kinetics of intracellular pH and phosphocreatine concentration after exercise in skeletal muscle was developed to calculate the rate of proton efflux in vivo.
2. Recovery of rat leg muscle pH after sciatic nerve stimulation was faster in spontaneously hypertensive rats than in Wistar-Kyoto controls (both n = 5).
3. Analysis of these data showed that the rate of proton efflux depends on intracellular pH, being greater at lower pH.
4. The early rate of proton efflux was greater in spontaneously hypertensive rats [measured over the first 0.8 min, 12.5 mmol min−1 kg−1 (sem 1.8) in spontaneously hypertensive rats compared with 7.6 mmol min−1 kg−1 (sem 0.4) in Wistar-Kyoto rats, P &lt; 0.05], even though pH at the start of recovery was higher [6.30 (sem 0.03) in spontaneously hypertensive rats compared with 6.17 (sem 0.01) in Wistar-Kyoto rats, P &lt; 0.01].
5. This novel analysis provides a quantitative estimate of the rate of proton efflux in vivo, and demonstrates directly that this is increased in spontaneously hypertensive rats, as has previously been inferred from pH changes during exercise and studies of cultured muscle cells in vitro.
An objective test for the diagnosis and grading of vasospasm in patients with Raynaud's syndrome
Authors: Allen Judith A. , Devlin Mark A. , McGrann Sean , Doherty Ciaran C. 
Published: August 2015

1. Reliable objective tests for the diagnosis and grading of vasospasm would be helpful in the assessment of patients with Raynaud's syndrome.
2. Measurements of finger blood flow at local finger temperatures from 32°C down to 20°C did not reliably distinguish between patients with Raynaud's syndrome and matched control subjects.
3. Using laser Doppler flowmetry to detect blood cell flux in fingertip skin, there was no significant difference (Wilcoxon's signed rank test) in the finger systolic blood pressure of 28 patients with Raynaud's syndrome and their matched controls when the fingers were warm at 32°C.
4. Absence of flux was considered to indicate complete vasospasm and the degree of cooling required to abolish flux indicated the severity of the vasospastic condition in an individual patient.
5. Finger cooling for 5 min did not significantly alter finger systolic blood pressure in the control subjects, but abolished blood cell flux in the fingertip skin of 27 of the 28 patients with Raynaud's syndrome.
6. A grading scale was derived from the flux measurements. There was a significant correlation (r=0.75, P &lt; 0.001) between the grading of disease severity as judged by the flux test and the clinical grade as assessed before the laboratory visit.
7. There was one false-negative result in the 28 patients with Raynaud's syndrome tested and no false-positive results in 28 matched control subjects.
8. This type of testing may prove helpful in the diagnosis and grading of vasospastic disorders.
Increases in NO2−/NO3− excretion in the urine as an indicator of the release of endothelium-derived relaxing factor during elevation of blood pressure
Authors: SUZUKI Hiromichi , IKENAGA Hideki , HISHIKAWA Keiichi , NAKAKI Toshio , KATO Ryuichi , SARUTA Takao 
Published: August 2015

1. Under hormonally constant conditions, the effects of a sudden increase in blood pressure on the release of endothelium-derived relaxing factor were evaluated by measuring urinary excretion of NO2−/NO3− in rats with renal denervation.
2. Elevation of blood pressure from 136 ± 2 to 153 ± 3 mmHg by an aortic clamp below the renal arteries induced a significant increase in urinary excretion of NO2−/NO3− from 76.6 ± 4.2 × 102 to 108.1 ± 8.3 × 102 pmol min−1 g−1 kidney weight (P &lt; 0.05).
3. Infusion of NG−monomethyl-L-arginine (1 mg min−1 kg−1) without an aortic clamp raised mean blood pressure to a similar level; however, urinary excretion of NO2−/ NO3− was decreased significantly.
4. During infusion of NG−monomethyl-L-arginine, aortic occlusion caused a significant increase in blood pressure without any changes in NO2−/NO3− excretion in the urine.
5. These results suggest that the formation of NO, an indicator of endothelium-derived relaxing factor release, was increased by mechanical pressure elevation without apparent changes in hormonal and neural factors.
Effect of simvastatin on plasma lipid and lipoprotein concentrations and low-density lipoprotein metabolism in the nephrotic syndrome
Authors: Warwick G. L. , Packard C. J. , Murray L. , Grierson D. , Stewart J. P. , Shepherd J. , Boulton-Jones J. M. 
Published: August 2015

1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia.
2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways.
3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%).
4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day−1 kg−1). Plasma lathosterol concentration was reduced in all eight patients (range 34–71%), indirectly confirming significant inhibition of cholesterol synthesis.
5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.
Cutaneous heat loss shortly after burn injury in children
Authors: Childs Charmaine , Stoner H. B. , Little R. A. 
Published: August 2015

1. Total heat loss and its components have been studied in cool (20°C) and warm (30°C) environments in 30 healthy children and 21 children who had been burned (10-17% body surface area) 0.5-29 h previously.
2. In healthy naked children at 20°C, the partition of total heat loss was: radiation, 64%; convection, 32%; evaporation, 4%. On transfer to the warm, total heat loss was reduced by approximately 50%, with disproportionate reductions in the contributions from radiation and convection being offset, to some extent, by an increase in evaporative heat loss.
3. In patients during the first 5.5 h after injury, the magnitude and pattern of heat loss at 20°C and 30°C were similar to those in control subjects and were unaffected by bandaging.
4. Ten to twenty-nine hours after injury, when the patients were bandaged and body temperature and heat content were significantly higher than in control subjects, radiant and convective heat losses were increased, but as evaporative heat loss tended to be reduced; total heat loss in the warm was unchanged. However, at this time at 20°C, total heat loss was reduced compared with healthy children at the same ambient temperature.
5. The findings of unchanged or reduced total heat loss and reduced evaporative heat loss in injured patients are interpreted as inappropriate responses to an increased body temperature and heat content in children after burn injury.
Raised resting energy expenditure in Parkinson's disease and its relationship to muscle rigidity
Authors: Markus H. S. , Cox M. , Tomkins A. M. 
Published: August 2015

1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded.
2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state.
3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.
Influence of circulating insulin-like growth factor-I compared with that of intrarenal insulin-like growth factor-I on proximal nephron receptor density in rats
Authors: Hise Michael K. , Corteza Quintina , Klassen David K. , Sadler John H. 
Published: August 2015

1. We examined the effects of dietary protein manipulations in partially nephrectomized (one and one-third nephrectomy) and normal rats to gain perspective on the relative importance of circulating versus intrarenal (collecting tubule) insulin-like growth factor-I in the control of proximal nephron receptor density. In addition, we studied the factors that influence liver insulin-like growth factor-I secretion in partially nephrectomized rats.
2. Dietary protein restriction (6% versus 40%) lowered circulating levels of insulin and insulin-like growth factor-I in both normal and partially nephrectomized rats up to 3 weeks after institution of the diets; however, growth hormone levels were little changed. Reduced renal mass stimulated intrarenal production of insulin-like growth factor I regardless of the diet.
3. Scatchard analysis revealed that the density of insulin-like growth factor-I receptors on glomerular and proximal tubule basolateral membranes increased when circulating levels of insulin-like growth factor-I were diminished, despite raised levels of intrarenal insulin-like growth factor-I, in partially nephrectomized rats.
4. Circulating insulin-like growth factor-I, rather than the tissue level, plays the dominant role in the control of proximal nephron receptor density under physiological conditions. Insulin, but not growth hormone, may play a role in liver insulin-like growth factor-I secretion in partially nephrectomized rats during dietary manipulations.