bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of different levels of briefly sustained ventricular pressure on arrhythmia in the isolated working rat heart
Authors: James M. A. , Jones J. V. 
Published: August 2015

1. The effect of different levels of ventricular pressure upon the prevalence of ventricular arrhythmias has been studied in 42 rat hearts by using the isolated working heart model.
2. The results have shown that there is an increased prevalence of arrhythmia at the highest levels of pressure tested in hearts from both normal and hypertensive rats. In hearts from normal rats total ectopic counts were 304 at 140 mmHg and 150 at 60 mmHg (P &lt; 0.05). In hearts from hypertensive rats total ectopic counts were 4217 at 180 mmHg and 2179 at 100 mmHg (P &lt; 0.05).
3. Hearts from hypertensive rats demonstrated significantly more ectopic activity than hearts from normal rats at all test pressures. Median values for ectopic counts for each study period were 68 in hearts from hypertensive rats and seven in hearts from normotensive rats (P &lt; 0.001).
4. There was evidence that the increased arrhythmia observed was not due to ischaemia or fatigue, and it seems likely that these effects of raised pressure are due to its effect on ventricular wall stress. The differences between various pressures were relatively small, but do suggest that a sustained increase in ventricular wall stress is arrhythmogenic.
5. This small arrhythmogenic effect over the relatively short period of these studies may be of much greater significance when considered in the context of the prolonged periods for which the diseased heart may be subjected to raised wall stress.
Arginine vasopressin attenuates phenylephrine-induced forearm vasoconstriction in men
Authors: Harada Seiki , Imaizumi Tsutomu , Momohara Michiko , Masaki Hiroyuki , Ando Shin-Ichi , Takeshita Akira 
Published: August 2015

1. The aim of this study was to examine whether arginine vasopressin modulates the vasoconstricting action of phenylephrine in human forearms.
2. In seven healthy subjects, we determined the percentage increases in forearm vascular resistance evoked by intra-arterial infusion of phenylephrine at graded doses during simultaneous intra-arterial infusion of saline or arginine vasopressin at two doses. Similarly, in another seven subjects, we examined the effects of intra-arterial infusions of saline or angiotensin II on the vasoconstricting action of intra-arterial phenylephrine.
3. Arginine vasopressin and angiotensin II caused small, but insignificant, increases in baseline forearm vascular resistance. Arginine vasopressin at the two doses significantly attenuated the percentage increases in forearm vascular resistance evoked with phenylephrine at graded doses. Angiotensin II did not alter the forearm vascular responses to phenylephrine.
4. Intra-arterial infusion of arginine vasopressin at doses of 0.6 and 1.8 ng/min raised the plasma arginine vasopressin concentration in the venous effluents from 1.6 ± 0.3 (control) to 4.0 ± 0.9 and to 16.4 ± 6.9 pg/ml, respectively.
5. These results suggest that arginine vasopressin at physiological concentrations with a minimal direct effect on resistance arteries attenuates the vasoconstricting action of phenylephrine in human forearms.
Metabolic balance studies of mineral supplementation in osteoporosis
Authors: Stamp Trevor , Katakity Monica , Goldstein A. J. , Jenkins M. V. , Kelsey C. R. , Rose G. A. 
Published: August 2015

1. We studied the effect of mineral supplementation and its duration is osteoporosis by analysing the calcium and phosphorus balances of 49 treated osteoporotic patients whose median length of calcium treatment was 19 weeks with a range of 8 days to over 4 years. Forty-four studies satisfied statistical criteria of reproducibility and included 35 women (10 also receiving oestrogen replacement therapy) and nine men.
2. Mean calcium balance was positive in women taking calcium supplements alone, +1.9 ± 2.5 mmol daily (P &lt; 0.002), and was significantly more positive (P &lt; 0.05) in women also taking oestrogens, +4.2 ± 2.1 mmol daily. Calcium balance was not significantly positive in men.
3. Calcium balance correlated negatively with duration of supplementation, but, significantly, only when duration of supplementation was expressed logarithmically (r = −0.401, P &lt; 0.01) giving the regression equation y = 4.2–1.6 log x, where y = calcium balance in mol/day and x = duration of supplementation in weeks. Theoretical net calcium retention, without allowance for dermal loss, could be calculated by integration.
4. Mean phosphorus balance was significantly positive in both groups of women and in the whole population. Although its correlation with duration of supplementation did not reach statistical significance (P &lt; 0.1), the ratio of the regression slopes for calcium and phosphorus, 1.5:1, corresponded to their molar ratio in bone.
5. These statistics are, we believe, the first to describe an exponential decline in calcium balance during mineral treatment of osteoporosis, but they firmly suggest that such treatment, with or without oestrogen therapy, conveys temporary benefit.
Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man
Authors: Kaye Gerald C. , Bayliss Peter , Lowry Philip J. , Drury P. L. , Camm A. John 
Published: August 2015

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia.
2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 ± 3 min, the mean group urine flow increased from 3.2 ± 2.3 ml/min to 7.6 ± 3.7 ml/min (P&lt;0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion.
3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 ± 4.6 pg/ml to 34.6 ± 21.7 pg/ml (P&lt;0.02) during the arrhythmia. There was no significant change in the plasma argininevasopressin level and a non-significant reduction in plasma renin activity.
4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vaso-pressin level alone.
A comparison of the pharmacological and mechanical properties in vitro of large and small pulmonary arteries of the rat
Authors: Leach R. M. , Twort C. H. C. , Cameron I. R. , Ward J. P. T. 
Published: August 2015

1. The mechanical and pharmacological properties of small pulmonary arteries (100–300 μm normalized lumen diameter) were directly compared with those of the left main pulmonary artery (1–2 mm) from the rat. The active and passive length-tension characteristics and responses to a variety of agonists and antagonists were dependent on arterial diameter.
2. Maximum contractile function was obtained in both groups of vessels when stretched so as to give an equivalent transmural pressure of 30 mmHg. This is substantially lower than that found for systemic vessels, and reflects the normal low pulmonary arterial pressure.
3. Noradrenaline was a powerful vasoconstrictor in large but not small pulmonary arteries (P&gt; 0.001). In contrast, bradykinin produced a significantly greater response in the small arteries (P &lt; 0.001). In comparison with large pulmonary arteries, small arteries were more sensitive to noradrenaline (P&lt;0.05) and 5-hydroxytryptamine (P &lt; 0.001), less sensitive to endothelin-1 (P&gt; 0.001) and had the same sensitivity to prostaglandin F2α.
4. The mechanism that maintains the low arterial tone of the pulmonary circulation is unknown, but it may involve the release of relaxing factors from the endothelium. In this preparation, basal resting tone could not be demonstrated in either large or small arteries.
5. Acetylcholine-induced relaxation of pre-contracted pulmonary arteries was reduced or absent in the small artery, despite histological evidence of an intact endothelium. In large arteries pre-contracted with prostaglandin F2α, acetylcholine (100 μmol/l) caused 88.2% relaxation compared with 25.2% in the small artery.
6. These results suggest that it would be unwise to extrapolate from results obtained either in large pulmonary artery preparations or in perfused lungs to what may occur in the functionally important resistance arteries.
Pressor response to a postural change in cirrhosis: an experimental study in the CCI4-treated rat
Authors: Bomzon Arieh , Weinbroum Avraham , Blendis Laurence M. 
Published: August 2015

1. Systemic hypotension, blunted cardiovascular responsiveness to noradrenaline and an abnormal hypertensive pressor response to a postural change have been described in cirrhotic patients.
2. We have examined the role of blunted responsiveness in these abnormalities by studying basal arterial blood pressure and its response to a postural change (vertical head-up 90° tilting) in conscious and pithed CCl4-treated (cirrhotic) rats, as well as assessing the pressor response to noradrenaline in vivo and the vascular contractile response to noradrenaline in vitro.
3. A diminished hypotensive response to a change in posture was found in pre-cirrhotic portal hypertensive rats, whereas an inverted hypertensive pressor response in the face of systemic hypotension occurred in the cirrhotic rats with portal hypertension.
4. The inverted pressor response was abolished in the pithed portal hypertensive cirrhotic rats.
5. The pressor response to noradrenaline in vivo in conscious cirrhotic rats and the vascular contractile responsiveness to noradrenaline in vitro were intact.
6. We conclude that blunted responsiveness to noradrenaline is not a contributory factor to the development of systemic hypotension or the inverted pressor response to a change in posture in cirrhosis.
Responsiveness of superficial hand veins to α-adrenoceptor agonists in insulin-dependent diabetic patients
Authors: Eichler Hans-Georg , Blaschke Terrence F. , Kraemer Fredric B. , Ford Gary A. , Blöchl-Daum Brigitte , Hoffman Brian B. 
Published: August 2015

1. Diabetic autonomic neuropathy causes loss of sympathetic cardiovascular control and is associated with increased vascular sensitivity to catecholamines. Supersensitivity to catecholamines could be due to either a postsynaptic increase in vascular sensitivity or to decreased catecholamine uptake into peripheral sympathetic nerve endings.
2. To differentiate between these possible mechanisms we have measured the responsiveness in vivo to noradrenaline and phenylephrine with local infusions into peripheral veins of diabetic patients with and without symptomatic autonomic neuropathy and of healthy control subjects. The dorsal hand vein compliance technique was used.
3. Symptomatic diabetic patients required significantly lower doses of noradrenaline for half-maximal venoconstriction (ED50) (geometric mean 2.14 ng/min) than control subjects (geometric mean 6.61 ng/min, P = 0.032), but there was no difference in the results from the phenylephrine dose-response curves between the groups. Thesre were no differences in venous responsiveness to noradrenaline or phenylephrine between the asymptomatic diabetic group and the control group. However, in the asymptomatic diabetic group, postural blood pressure change (an index of loss of sympathetic control) was correlated with the ED50 for noradrenaline (r = 0.74, P = 0.014), but not with the ED50 for phenylephrine. In the control group the ED50 values for noradrenaline and phenylephrine were correlated with each other (r= 0.81, P= 0.0005).
4. Both vasopressor drugs act on vascular α-adrenoceptors, but only noradrenaline is taken up into peripheral sympathetic nerve endings. Our results suggest that, in diabetic patients, vascular supersensitivity to catecholamines is primarily determined by decreased neuronal catecholamine uptake. A postsynaptic increase in vascular a-adrenoceptor stimulation does not appear to be prominent in diabetic autonomic neuropathy.
Vascular responses and ion exchange in diabetes
Authors: Wardle E. N. 
Published: August 2015

The use of erythrocyte Na+/Li+ countertransport as a gold standard, as in the article by Halkin et al. (Clin. Sci. 1991; 81, 223–32) [1], should give rise to disquiet because it has been known for a long time that this parameter is influenced by low-density lipoprotein (LDL), by cholesterol and by saturated fatty acids. Recently, it has been clarified that LDL increases the Vmax of this flux [2]. One has to agree that it is interesting that there is an inverse relationship between the ability to dilate blood vessels and Na+/Li+ exchange in the diabetic patient, but actually the basis for this apparent relationship is already known and it is not quite as direct as the authors might wish to imply.
It is not native LDL but oxidized LDL [3] that stops the formation of endothelium-derived relaxing factor (EDRF) [4], reduces prostacyclin production and even enhances ‘tissue factor' formation by endothelial cells [5]. In fact, the reduced production of EDRF by diabetic patients that is pertinent to atherogenesis can be correlated with a raised plasma level of cholesterol [6] and also with the plasma level of lipid peroxides [7].
In that case there is some basic information missing concerning the effects of lipid peroxides on Na+/Li+ fluxes in erythrocytes. When this is known, it might well explain why this parameter seems to relate to hypertension and/or nephropathy in diabetic patients.
Meantime, in a study of this kind [1] we should have been told which of the subjects were smokers, especially as there were two outstanding points on each graph that formed the relationship.
α-Adrenoceptor blockade by phentolamine inhibits adrenaline-induced platelet activation in vivo without affecting resting measurements
Authors: Larsson P. T. , Wallén N. H. , Egberg N. , Hjemdahl P. 
Published: August 2015

1. The effects of phentolamine (500 μg/min) on platelet aggregability in vivo at rest and during adrenaline infusion were assessed by ex vivo filtragometry and measurements of plasma β-thromboglobulin levels in 10 healthy male subjects. Plasma levels of von Willebrand factor antigen and free fatty acids were also measured.
2. Adrenaline induced marked and expected increases in heart rate and systolic blood pressure and decreased diastolic blood pressure when venous plasma adrenaline levels were elevated from 0.12 ± 0.02 to 2.9 ± 0.3 nmol/l (P &lt; 0.01).
3. Adrenaline caused platelet activation in vivo. Ex vivo filtragometry readings were shortened by 58 ± 9% (P &lt; 0.01), plasma β-thromboglobulin levels increased by 99 ± 44% (P &lt; 0.01) and platelet counts increased by 26 ± 6% (P &lt; 0.01). Plasma levels of von Willebrand factor antigen and free fatty acids increased by 53 ± 5% and 475 ± 113% (both P &lt; 0.01), respectively.
4. Phentolamine enhanced the β-adrenergic vasodilator responses to adrenaline, as both the decrease in diastolic blood pressure and the reflexogenic increase in heart rate were enhanced (both P &lt; 0.01). Marked elevations in plasma noradrenaline levels were found during infusions of phentolamine and adrenaline (P &lt; 0.001).
5. Phentolamine did not alter platelet indices at rest, but abolished adrenaline-induced platelet activation, as filtragometry readings, plasma β-thromboglobulin levels and platelet counts remained at, or below, resting levels. Responses of plasma levels of von Willebrand factor antigen and free fatty acids to adrenaline were not influenced by phentolamine and did not seem to influence platelet responses.
6. Thus, platelet activation by adrenaline in vivo is mediated via α-adrenoceptors, apparently with minor influences of other physiological responses. Circulating and/or locally released catecholamines may activate platelets directly via α-adrenoceptor stimulation during stressful physiological and pathophysiological conditions in humans.
Platelet cytosolic free calcium concentration and parathyroid hormone: changing relationships with haemodialysis in end-stage renal disease
Authors: Fluck R. J. , McMahon A. C. , Alameddine F. M. , Dawnay A. B. S. , Baker L. R. I. , Raine A. E. G. 
Published: August 2015

1. Twelve patients receiving haemodialysis for end-stage renal failure were studied at a single dialysis session. Platelet cytosolic calcium concentration, plasma ionized calcium concentration and serum parathyroid hormone concentration were measured before dialysis, mid-dialysis and 30 min after dialysis.
2. Plasma ionized calcium concentration increased towards dialysate calcium concentrations, falling insignificantly after cessation of dialysis. Serum parathyroid hormone concentration fell by 39% during dialysis, with incomplete recovery afterwards. There was no overall change in platelet cytosolic calcium concentration.
3. Patients were divided into two subgroups: low parathyroid hormone (serum parathyroid hormone concentration &lt; 10 pmol/l) and high parathyroid hormone (serum parathyroid hormone concentration &gt; 10 pmol/l). Before dialysis, values of platelet cytosolic calcium concentration or plasma ionized calcium concentration were not statistically different between the subgroups, but the platelet cytosolic calcium concentration was higher in the high-parathyroid hormone subgroup during and after dialysis.
4. Before haemodialysis there was a linear correlation between plasma ionized calcium concentration and platelet cytosolic calcium concentration, which disappeared during dialysis. In contrast, there was no relationship between serum parathyroid hormone concentration and platelet cytosolic calcium concentration before dialysis, but after dialysis a hyperbolic relationship was evident.
5. These results suggest that uraemic toxins may interfere with cytosolic calcium homoeostasis, allowing passive diffusion of extracellular calcium to influence the resting concentration, and that this effect is reversible by haemodialysis.
Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies
Authors: Bouhnik J. , Richoux J. P. , Huang H. , Savoie F. , Baussant T. , Alhenc-Gelas F. , Corvol P. 
Published: August 2015

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques.
2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats.
3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets.
4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different.
5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet.
6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.
Atrial natriuretic peptide inhibits fluid intake in hyperosmolar subjects
Authors: Burrell Louise M. , Palmer J. M. , Baylis P. H. 
Published: August 2015

1. The effect of atrial natriuretic peptide on osmotically stimulated thirst appreciation and consequent fluid intake was investigated in healthy man.
2. Six seated male subjects were studied on two occasions: synthetic α-human atrial natriuretic peptide (99–126) (2 pmol min−1kg−1) or placebo (saline, 150 mmol/l NaCl) was infused intravenously for 105 min; 30 min after the start of atrial natriuretic peptide/placebo infusion, hypertonic saline (855 mmol/l NaCl) was infused (0.06 ml min−1 kg−1) for 60 min. Subjects were then allowed free access to water for the next 2 h; infusion of atrial natriuretic peptide/ placebo continued for the first 15 min of the drinking period.
3. The plasma atrial natriuretic peptide concentration did not alter significantly during infusion of hypertonic saline and placebo; it rose to a steady state of 12.7 ± 1.1 pmol/l (mean ± SEM) during the infusion of atrial natriuretic peptide and hypertonic saline, and remained at this level during the first 15 min of the drinking period. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, similar increases in plasma osmolality (P &lt; 0.001) and plasma vasopressin concentration (P &lt; 0.005) occurred. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, thirst increased significantly over the time course of both studies (P&lt;0.01), but the effect of atrial natriuretic peptide infusion compared with placebo infusion was to significantly decrease thirst at 60 min.
4. Drinking rapidly abolished thirst and vasopressin secretion before changes in plasma osmolality occurred. Subjects drank significantly less water after atrial natriuretic peptide infusion compared with after placebo infusion (P&lt;0.01).
5. In conclusion, physiological increases in plasma atrial natriuretic peptide concentrations blunt osmotically stimulated thirst appreciation and attenuate subsequent fluid intake in hyperosmolar man.