bluuebunny/crossref_metadata_2025_split huggingface dataset:
Granulocyte margination in the human lung and its response to strenuous exercise
Authors: Peters A. M. , Allsop P. , Stuttle A. W. J. , Arnot R. N. , Gwilliam M. , Hall G. M. 
Published: August 2015

1. It is widely believed that the lung is an important site of granulocyte margination and releases most of the granulocytes of the peripheral neutrophilia of exercise.
2. We measured granulocyte margination in the lung in terms of the lung total blood granulocyte pool and the lung circulating granulocyte pool in eight patients without inflammatory disease or evidence of lung pathology by comparing the regional γ-camera lung count rate of 111In-labelled granulocytes with that of 111In-labelled erythrocytes. According to the respective 111In activities in peripheral blood samples taken between 5 and 40 min after granulocyte injection, the lung marginating granulocyte pool was 0.78 (sem 0.045) of the lung total blood granulocyte pool or 4.6 (0.92) of the lung circulating granulocyte pool 5 min after injection, decreasing to plateau values of 0.57 (0.053) and 1.53 (0.28) from 20 min after injection. This compared with corresponding whole-body ratios of about 0.6 and 1.5, respectively.
3. After 4 min of maximal exercise in four normal subjects given 111In-labelled granulocytes 60 min before exercise, the 111In-labelled granulocyte count rate over the lung increased to 1.23 (0.05) of the pre-exercise value with a time course that was essentially identical with the time course of the peripheral native neutrophilia. The spleen 111In signal decreased with the same time course, reaching a minimum of 0.63 (0.05) of the pre-exercise level at 5–10 min after the end of exercise.
4. In a further four normal subjects given 99mTc-labelled erythrocytes, exercise resulted in an increase in the lung 99mTc count rate to 1.11 (0.05) of the pre-exercise value. This increase was maximal immediately after the end of exercise. Based on changes in peripheral haemoglobin, total blood volume decreased in the eight normal subjects to 0.89 (0.01) of the pre-exercise value.
5. Using (a) the mean increases seen in lung 111In and 99mTc count rates in the normal subjects, (b) the mean haemoconcentration recorded in the normal subjects and (c) the mean baseline ratio of lung marginating granulocyte pool/lung total blood granulocyte pool measured in the patients, we calculated that the lung marginating granulocyte pool after exercise declined to only 0.94 of the pre-exercise value in the four normal subjects given 111In-labelled granulocytes.
6. We conclude (a) that although granulocytes marginate in the lung, they do not do so to an extent greater than the average for the whole body, and (b) that there is no significant release of granulocytes from the lungs as a result of exercise.
Plasma levels of endothelin in chronic renal failure and after renal transplantation: Impact on hypertension and cyclosporin A-associated nephrotoxicity
Authors: Stockenhuber F. , Gottsauner-Wolf M. , Marosi L. , Liebisch B. , Kurz R. W. , Balcke P. 
Published: August 2015

1. Plasma levels of endothelin were measured in 30 patients with chronic renal failure, 32 patients on chronic haemodialysis treatment and 25 renal graft recipients with stable renal graft function.
2. In patients with chronic renal failure as well as in patients on regular haemodialysis treatment, mean plasma levels of endothelin were significantly increased (4.59 ± 2.09 pg/ml, 10.08 ± 3.12 pg/ml, respectively) when compared with normal subjects (1.88 ± 0.6 pg/ml, P &lt;0.01, P &lt;0.001, respectively).
3. In the group with chronic renal failure a positive correlation between the plasma level of endothelin and the plasma concentration of creatinine was observed (P&lt;0.003).
4. Renal graft recipients on cyclosporin A with stable renal graft function had a normal plasma level of endothelin suggesting that cyclosporin A nephrotoxicity is not mediated by endothelin.
5. Hypertensive patients with chronic renal failure or on regular haemodialysis and hypertensive renal graft recipients did not differ from the corresponding normotensive population with regard to the plasma level of endothelin, demonstrating that an increased plasma level of endothelin does not play a major role in the pathogenesis of renal hypertension.
Renal, haemodynamic and hormonal interactions between atrial natriuretic factor and arginine vasopressin in patients with congestive heart failure
Authors: Nakamura Motoyuki , Yoshida Hiroaki , Funakoshi Tsutomu , Arakawa Naoshi , Hiramori Katsuhiko 
Published: August 2015

1. Nine patients with compensated heart failure were infused with synthetic arginine vasopressin at a rate of 0.1 m-units min−1 kg−1 for 60 min to increase their plasma arginine vasopressin concentration. Synthetic human atrial natriuretic factor (3 pmol min−1 kg−1) or placebo was co-infused with the arginine vasopressin in random order in a single-blind cross-over design.
2. The resultant plasma concentrations of arginine vasopressin and atrial natriuretic factor fell to within the upper range observed in congestive heart failure. Compared with the infusion of arginine vasopressin alone, atrial natriuretic factor co-infusion enhanced both the urine flow rate and the sodium excretion rate (both P &lt; 0.05) without significant haemodynamic and hormonal effects.
3. Systematic blood pressure was elevated by arginine vasopressin infusion (P &lt; 0.05) without any change in heart rate. Co-infusion of atrial natriuretic factor did not affect these haemodynamic parameters.
4. These results suggest that an increased release of atrial natriuretic factor maintains water and sodium excretion in the presence of arginine vasopressin-induced renal modulations, and that the pressor effect of arginine vasopressin is not antagonized by the increased plasma level of atrial natriuretic factor in patients with congestive heart failure.
Longitudinal study of platelet angiotensin II binding in human pregnancy
Authors: Baker Philip N. , Pipkin Fiona Broughton , Symonds E. Malcolm 
Published: August 2015

1. Platelet angiotensin II binding, circulating angiotensin II levels, plasma renin substrate and plasma renin concentration were measured in a longitudinal study of 30 women during pregnancy and the puerperium.
2. There was a significant fall in platelet angiotensin II binding from 11 weeks gestation to 18 weeks gestation (P &lt; 0.01). There were no further significant changes in platelet angiotensin II binding until after delivery, a significant rise in platelet angiotensin II binding being found at 6 weeks post partum as compared with at 36 weeks gestation (P &lt; 0.01). There was no further significant change from 6 to 12 weeks post partum, and platelet angiotensin II binding at 6 and 12 weeks post partum in the pregnant cohort approximated to that in non-pregnant women. These changes parallel those known to occur in pressor responsiveness to angiotensin II in pregnancy.
3. Plasma angiotensin II concentration, plasma renin substrate and plasma renin concentration were all significantly higher during pregnancy than in the puerperium (P &lt; 0.001). There were no significant changes during pregnancy in plasma angiotensin II concentration or plasma renin concentration, although plasma renin substrate rose throughout.
4. Significant inverse correlations between platelet angiotensin II binding and plasma angiotensin II concentration (P &lt; 0.01), plasma renin substrate (P &lt; 0.01) and plasma renin concentration (P 0&gt;001) were found during pregnancy. These data suggest that down-regulation of platelet angiotensin II binding by the components of the renin-angiotensin system pertains in pregnancy.
5. We are currently investigating parallelism between platelet and vascular angiotensin-binding sites. If such is confirmed, studies of platelet angiotensin II binding in pregnancy may be of both basic physiological and clinical interest in relation to the hypertensive diseases of pregnancy.
Dose-response study of the redistribution of intravascular volume by angiotensin II in man
Authors: Motwani Joseph G. , Struthers Allan D. 
Published: August 2015

1. The response of systemic and regional haemodynamic indices to increasing infusion rates of angiotensin II (1, 3 or 10 ng min−1 kg−1) or placebo [5% (w/v) d-glucose] was studied in eight normal male subjects.
2. As compared with placebo, angiotensin II infusion caused an incremental rise in the serum angiotensin II level [14.5 ± 7.7 (placebo) to 187.2 ± 36.1 (10 ng of angiotensin II min−1 kg−1) pmol/l; mean ± 95% confidence interval] associated with a stepwise increase in total peripheral resistance [880 ± 42 (placebo) to 1284 ± 58 (10 ng of angiotensin II min−1 kg−1) dyn s cm−5] and a progressive reduction in cardiac output [8.3 ± 0.4 (placebo) to 7.0 ± 0.4 (10 ng of angiotensin II min−1 kg−1) litres/min].
3. A stepwise fall in renal blood flow was observed with increasing angiotensin II infusion rate [1302 ± 65 (placebo) to 913 ± 64 (10 ng of angiotensin II min−1 kg−1) ml/min]. In contrast, calf blood flow was unaffected by 1 ng or 3 ng of angiotensin II min−1 kg−1 and was significantly increased by 10 ng of angiotensin II min−1 kg−1 (P &lt; 0.01).
4. Calf venous capacitance was uninfluenced by 1 ng of angiotensin II min−1 kg−1, but was significantly increased by both 3 ng (P &lt; 0.005) and 10 ng (P &lt; 0.001) of angiotensin II min−1 kg−1.
5. Our results indicate that the pressor response to angiotensin II is a summation of multiple regional haemodynamic effects which differ qualitatively not only with the vascular bed studied but also within a single tissue, with the level of circulating angiotensin II attained.
6. The venodilatation we have demonstrated with high angiotensin II levels may effect a potentially favourable redistribution of blood flow in situations of inappropriate extracellular fluid volume expansion, such as chronic heart failure.
Effect of oral lithium on bronchial reactivity in asthma
Authors: Knox A. J. , Higgins B. G. , Hall I. P. , Tattersfield A. E. 
Published: August 2015

1. Recognition that inositol phospholipid-derived second messengers are involved in the initiation and maintenance of airway smooth muscle contraction raises the possibility of new therapeutic approaches to the treatment of asthma. We anticipated that lithium, through its effects on cell signal transduction and ion-transport pathways, would be likely to protect the airways against constrictor stimuli.
2. We carried out a randomized, double-blind study of lithium carbonate in asthmatic patients.
3. After a 1 week run-in period, 27 patients were allocated lithium carbonate (800 mg) or placebo for 21 days with measurement of forced expiratory volume in 1 s, the dose of histamine causing a 20% fall in the forced expiratory volume in 1 s and serum lithium concentration on days 3, 7, 14 and 21.
4. Twenty-one patients completed the study (10 on lithium, 11 on placebo). Mean serum lithium levels for patients on active treatment were in the therapeutic range on all four occasions.
5. Lithium did not alter the forced expiratory volume in 1 s (P=0.8) or the twice-daily peak expiratory flow (P=0.15). It did, however, reduce histamine reactivity (the maximum difference between lithium and placebo was 1.2 doubling doses of histamine on day 21; 95% confidence interval 0.2–2.2 doubling doses), improve symptom scores (P &lt; 0.05) and reduce usage of β-adrenoceptor agonist inhalers (P &lt; 0.05).
6. We conclude that lithium reduces bronchial reactivity in airway smooth muscle; this finding raises new therapeutic possibilities for the treatment of asthma.
Effects of xylitol- and/or glutamine-supplemented parenteral nutrition on septic rats
Authors: Salleh M. , Ardawi M. 
Published: August 2015

1. The effects of parenteral nutrition with or without xylitol and/or glutamine supplementation were studied in septic rats after 4 days of treatment.
2. Septic rats treated with xylitol- and/or glutamine-supplemented parenteral nutrition survived sepsis significantly better than other parenteral nutrition-treated septic rats: the cumulative percentage of deaths over 4 days in septic rats treated with xylitol-glutamine-supplemented parenteral nutrition was 9.5% compared with 54.5% in septic rats given parenteral nutrition without xylitol and glutamine, and 52.4% in septic rats treated with parenteral nutrition supplemented with glucose.
3. Xylitol- and/or glutamine-supplemented parenteral nutrition resulted in improved nitrogen balance in septic rats: the cumulative nitrogen balance over the 4 days of treatment was positive in the rats given xylitol-supplemented parenteral nutrition and more positive when rats were treated with xylitol-glutamine-supplemented parenteral nutrition, as compared with other groups of septic rats.
4. The rate of loss of intracellular glutamine in skeletal muscle was markedly decreased (P &lt; 0.001) in response to xylitol- and/or glutamine-supplemented parenteral nutrition in septic rats.
5. Hepatic protein and RNA contents were increased in septic rats treated with xylitol- and/or glutamine-supplemented parenteral nutrition. Similarly, protein and RNA contents were markedly increased in muscles of septic rats treated with xylitol- and/or glutamine-supplemented parenteral nutrition.
6. The rates of incorporation of leucine/tyrosine into liver/muscle proteins in vitro were increased and the rate of muscular tyrosine release was decreased in response to xylitol- and/or glutamine-supplemented parenteral nutrition in septic rats.
7. It is concluded that the administration of xylitol- and/ or glutamine-supplemented parenteral nutrition is beneficial to septic rats and possibly to septic patients.
Effects of oral contraceptives containing oestrogen combined with norethisterone or levonorgestrel on erythrocyte cation transport in normal women
Authors: Stokes G. S. , Monaghan J. C. , Flemming C. L. , Johnston H. , Jones M. , Pinkerton G. , Baber R. 
Published: August 2015

1. Studies were undertaken in pre-menopausal women to examine the effects of treatment with standard oestrogen-progestogen and progestogen-only oral contraceptives on erythrocyte Na+,K+ co-transport and Na+−Na+ countertransport over 3- and 6-month periods. Concurrent observations were made on other erythrocyte cation transport components, plasma lipid concentrations, plasma renin activity, plasma aldosterone concentration and blood pressure.
2. Na+,K+ co-transport, measured as the ouabain-resistant, frusemide-sensitive component of 86Rb+ influx, and Na+−Na+ countertransport, measured as the ouabain-resistant, phloretin-sensitive component of 22Na+ influx, were both increased in women taking, on days 1–21 of their cycle, ethinyloestradiol (30–50 μg) combined with norethisterone (1000 μg or 500–1000 μg) for 3 or 6 months. Neither of these fluxes was increased in a control group of women, or in women treated for the same time periods with ethinyloestradiol combined with levonorgestrel.
3. In a separate study of erythrocyte cation transport (excluding Na+−Na+ countertransport), in which women undertook treatment with norethisterone only (350 μg/ day) for 6 months starting 6 weeks post partum, no changes in Na+,K+ co-transport were observed at 3 or 6 months; there were no changes in cation transport in a corresponding control group.
4. The results of these studies confirm that certain oral contraceptive compounds can alter erythrocyte cation transport, and indicate that norethisterone in higher dose preparations is the component predominantly responsible. The alterations observed could not be explained by a direct link with concurrent changes in plasma triacylglycerol concentrations or in the renin-aldosterone axis and were not closely associated with elevation of blood pressure.
Lithium pretreatment affects renal and systemic responses to angiotensin II infusion in normal man
Authors: Eadington D. W. , Freestone S. , Waugh C. J. , Swainson C. P. , Lee M. R. 
Published: August 2015

1. Renal and systemic responses to infusion of angiotensin II (1.25 and 2.5 ng min−1 kg−1 body weight) were examined in ten normal males 12 h after single doses of 750 mg of lithium carbonate, 250 mg of lithium carbonate (n = 6) or placebo.
2. Baseline mean arterial pressure [mean (sem)] was higher after 750 mg of lithium [93.1 (1.7) versus 89.5 (1.9) mmHg, P = 0.014], and the subsequent rise in blood pressure during angiotensin II infusion was lower [8.2 (1.8) versus 12.2 (2.4) mmHg, P &lt; 0.02].
3. Lithium at a dose of 750 mg increased overnight urinary sodium excretion before the study. The fall in fractional sodium excretion during angiotensin II infusion was reduced after pretreatment with 750 mg of lithium [750 mg of lithium, 2.73 (0.24) to 1.34 (0.08)%; placebo, 2.69 (0.26) to 1.01 (0.11)%; P=0.02]. The increases in effective filtration fraction [750 mg of lithium, 5.4 (1.0)%; placebo, 8.6 (0.7)%; P &lt; 0.05] and total effective renal vascular resistance [750 mg of lithium, 3700 (390) dyn s cm−5; placebo 5100 (460) dyn s cm−5; P=0.03] during angiotensin II infusion were also attenuated after 750 mg of lithium. Responses after 250 mg of lithium did not differ from those after placebo.
4. The fall in plasma renin activity and the increase in plasma aldosterone concentration during angiotensin II infusion were similar on each study day.
5. Renal responses to exogenous angiotensin II are altered after pretreatment with a 750 mg dose of lithium in normal man. This dose of lithium is not an inert marker of sodium handling.
Altered renal response to enhanced endogenous 5-hydroxytryptamine after tryptophan administration in essential hypertension
Authors: Tomoda Fumihiro , Takata Masanobu , Oh-Hashi Shinya , Ueno Hitoshi , Yasumoto Kotaro , Iida Hiroyuki , Sasayama Shigetake 
Published: August 2015

1. To examine the pathophysiological significance of 5-hydroxytryptamine (serotonin) in essential hypertension, we compared the renal response to intrarenally formed 5-hydroxytryptamine by oral dosing with its precursor, L-tryptophan (2 g), in nine patients with essential hypertension and in six subjects with normotension.
2. Before tryptophan administration, urinary excretion of 5-hydroxytryptamine was significantly higher in the hypertensive group than in the normotensive group (66 ± 8 versus 36 ± 6 ng/min, P &lt; 0.05), whereas renal plasma flow and glomerular filtration rate did not differ between the two groups. After dosing with tryptophan, urinary excretion of 5-hydroxytryptamine significantly increased to the same plateau level in both groups (366 ± 55 ng/min in the hypertensive group and 365 ± 64 ng/min in the normotensive group). Significant and equivalent decreases in renal plasma flow were observed in the early phase after tryptophan administration in both groups (−8.5 ± 3.4% in the hypertensive group and −8.2 ± 1.7% in the normotensive group). Thereafter, renal plasma flow increased to above the baseline value in normotensive subjects, whereas this late vasodilatation was absent in the hypertensive group. Glomerular filtration rate significantly decreased at the time of the fall in renal plasma flow in the normotensive group (106.8 ± 7.8 to 92.7 ± 8.5 ml min−1 1.73 m−2, P &lt; 0.05), whereas it remained unchanged in the hypertensive group (108.2 ± 6.2 to 110.4 ± 6.3 ml min−1 1.73 m−2, not significant). Consequently, the filtration fraction did not change in normotensive subjects (0.21 ± 0.01 versus 0.19 ± 0.01, not significant), but it increased significantly in the hypertensive group (0.22 ± 0.01 versus 0.26 ± 0.02, P &lt; 0.05). A similar sustained antidiuresis was also observed after tryptophan administration in both groups. In addition, the above-described renal functional changes were not accompanied by any significant changes in systemic blood pressure, the renin-angiotensin-aldosterone system, adrenergic activity or plasma 5-hydroxytryptamine concentration in either group.
3. Our data show that in essential hypertension there is a baseline overproduction of renal 5-hydroxytryptamine, which may contribute to a reduction in renal excretory capability. The altered renal response to tryptophan found in essential hypertension may be partly related to the exaggerated efferent arteriolar constriction induced by endogenously formed 5-hydroxytryptamine.
Effect of bicarbonate administration on skeletal muscle intracellular pH in the rat: implications for acute administration of bicarbonate in man
Authors: Thompson Campbell H. , Syme Paul D. , Williams E. Mark , Ledingham John G. G. , Radda George K. 
Published: August 2015

1. The effect of bicarbonate administration on the intracellular pH of rat skeletal muscle was examined by using 31P n.m.r.
2. Bicarbonate administered intraperitoneally caused a significant intracellular acidosis in rat skeletal muscle in vivo. When the bicarbonate was administered intravenously there was no such change in the pH of the skeletal muscle.
3. Bicarbonate administration by either route resulted in an elevated mixed venous partial pressure of carbon dioxide and an elevated arterial pH, but no significant change in the arterial partial pressure of carbon dioxide. The increase in arterial bicarbonate concentration after intraperitoneal injection of bicarbonate was delayed when compared with that after intravenous injection.
4. The administration of hypertonic solutions intravenously caused a transient 40–50% fall in blood pressure, which had resolved within 1 min.
5. The data suggest that the effect of bicarbonate administration on intracellular pH in vivo is related not only to carbon dioxide loading of the cell but also to the rate of change in the extracellular bicarbonate concentration.