bluuebunny/crossref_metadata_2025_split huggingface dataset:
Study of the Electrophysiological Effects of Early or Subendocardial Ischaemia with Intracavitary Electrodes in the Dog
Authors: Donaldson R. M. , Taggart P. , Nashat F. , Abed J. , Rickards A. F. , Noble D. 
Published: August 2015

1. The early electrophysiological patterns of regional subendocardial ischaemia were studied by using the paced endocardial evoked response and simultaneous endocardial monophasic action potential recordings in 16 experiments in open chested dogs. Ischaemia was produced by transient (1-3 min) coronary artery occlusion.
2. Regional subendocardial isochaemia caused asynchronous activation due to differential conduction delay and shortened repolarization as evaluated by the duration of the paced evoked response from 175±(sd) 18.7 ms to 167 ± 16 ms (P &lt;0.001). These changes occurred within 60 s of occlusion and reversed rapidly after release of the occlusion.
3. In simultaneous endocardial monophasic action potentials there was a decrease in plateau amplitude and the duration of repolarization shortened from 180±(sd) 21.2 ms to 167 ±20.4 ms (P &lt;0.001).
4. The delay in endocardial activation after 2 min ischaemia was 5.5 ms, which is considerably shorter than the conduction delay previously reported in the subepicardial layers.
5. The calcium-channel blocking drug verapamil (infused at 0.4 mg/kg) altered the rate at which shortening of repolarization and asynchronous activation occurred during ischaemia in six experiments.
6. These experiments suggest that intracavitary electrodes could provide earlier and more sensitive detection of regional subendocardial ischaemia and may permit the assessment of therapy on the early electrical changes in the intact heart.
The Effects of Captopril on Blood Pressure, Urinary Water and Electrolyte Excretion and Drinking Behaviour in Brattleboro Rats
Authors: Gardiner Sheila M. , Bennett T. 
Published: August 2015

1. The effects of the orally active converting enzyme inhibitor, captopril (SQ 14225), on blood pressures and intakes and urine outputs of water and electrolytes were studied in rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) and in Long Evans rats (parent strain).
2. Captopril given in the drinking water (30 mg day−1 kg−1) caused an increase in fluid intake and urine output in both strains of rat; the difference between intake and measured output did not change.
3. Captopril caused a significant natriuresis wnen given to animals in the non-steady state but did not significantly affect the urinary electrolyte excretion of animals in a steady state; in the latter group, however, captopril caused a significant reduction in food intake. Hence, under both conditions, captopril caused a reduction in sodium balance.
4. Systolic blood pressures were reduced by captopril (given in the drinking water) in Long Evans rats and in Brattleboro rats; there was no accompanying change in heart rate.
5. Bolus administration of captopril (30 mg day−1 kg−1) either intragastrically or subcutaneously did not change the fluid intakes or outputs in either strain of rat.
6. In a separate experiment, rats were given the choice to drink water or a captopril solution. The results showed that the increased fluid intake in response to captopril was not due to a liking for the taste of the solution.
7. The dipsogenic response to captopril may have been due to the fall in blood pressure which occurred, leading to renin release and a peripheral build-up of angiotensin I, which was converted into angiotensin II in the central nervous system. The possibility that the same dose given as a bolus may have inhibited central, as well as peripheral, converting enzyme activity is discussed.
Importance of Platelet-Free Preparations for Evaluating Lymphocyte Nucleotide Levels in Inherited or Acquired Immunodeficiency Syndromes
Authors: Goday A. , Simmonds H. A. , Webster D. R. , Levinsky R. J. , Watson A. R. , Hoffbrand A. V. 
Published: August 2015

1. Low ATP/ADP ratios have been reported consistently for nucleotide levels of mononuclear cells separated from peripheral blood by conventional techniques.
2. We have established that these low values (mean 2.3:1) were not due to cell damage or poor viability, but resulted from heavy platelet contamination, which is unavoidable when heparinized blood is used. The results reflect the low ATP/ADP ratios (mean 1.6:1) characteristic of platelets. Platelet-free extracts from defibrinated blood had very high ATP/ADP ratios (mean 17.4:1).
3. The initial finding of detectable amounts of deoxy-ATP and deoxy-GTP in mononuclear cells from children with two distinct inherited immunodeficiency disorders [adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) deficiency respectively] many have been due to contamination by nucleated erythrocytes as well as platelets in non-defibrinated preparations.
4. Defibrination before nucleotide extraction of mononuclear cells from a patient with T-cell leukaemic/lymphoma treated with the ADA inhibitor deoxycoformycin enabled the demonstration of grossly raised deoxy-ATP levels relative to deoxy-ADP levels (ratio 16.1:1), associated with severe ATP depletion. This reciprocal relationship between ATP and dATP was found by us previously in the erythrocytes in inherited ADA deficiency.
5. These findings underline the importance of extracts uncontaminated by platelets, or nucleated erythrocytes, in the evaluation of lymphocyte nucleotide levels in inherited or acquired immunodeficiency syndromes.
Effect of Adrenergic and Vagal Blockade on the Normal Human Airway Response to Exercise
Authors: Warren J. B. , Jennings S. J. , Clark T. J. H. 
Published: August 2015

1. Ten normal, non-asthmatic subjects performed an 18 min graduated exercise test on a static exercise bicycle on 3 separate days. They received either no medication, or propranolol 80 mg orally 2 h before, or ipratropium bromide 0.216 mg by inhalation 30 min before, the start of exercise.
2. With no medication, transpulmonary index (TPI), a measure of airway resistance, fell linearly during exercise from a resting value of 0.269 ± 0.024 to 0.170 ± 0.014 kPa·1−1·s by the end of exercise. This returned to baseline between 2 and 4 min after stopping exercise.
3. Propranolol elevated baseline TPI slightly from 0.270 ± 0.024 to 0.294 ± 0.024 before exercise and during exercise this fell linearly to 0.185 ± 0.016 kPa·1−1·s. The fall in TPI during exercise after propranolol was not significantly different from the fall seen with no medication. Six minutes after exercise stopped TPI rose to 0.336 ± 0.035 kPa·1−1·s after propranolol. All values for TPI from 4 min to 16 min after exercise were significantly higher after propranolol than the corresponding values found after no medication (P&lt;0.05).
4. Ipratropium bromide decreased baseline TPI from 0.264 ± 0.024 to 0.163 ± 0.013 kPa·1−1·s (P&lt;0.001) and this did not change significantly further either during or after exercise.
5. Normal subjects show considerable airway dilatation during exercise and this appears to result from inhibition of resting vagal tone. The sympathetic system does not appear to mediate the airway dilatation during exercise, but it may be important in protecting against post-exercise bronchoconstriction.
Calcium Malabsorption in Elderly Women with Vertebral Fractures: Evidence for Resistance to the Action of Vitamin D Metabolites on the Bowel
Authors: Francis R. M. , Peacock M. , Taylor G. A. , Storer J. H. , Nordin B. E. C. 
Published: August 2015

1. Radio-calcium absorption, plasma 25-hydroxyvitamin D [25-(OH)D] and 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were measured in 19 elderly women with, and 21 without, vertebral fractures, before and after treatment with 25-hydroxyvitamin D3 [25-(OH)D3], to establish whether malabsorption of calcium in elderly women with vertebral fractures has a cause different from that in elderly women without vertebral fractures.
2. Malabsorption of calcium and low plasma 25-(OH)D and 1,25-(OH)2D concentrations were common in both groups of women but there was no significant difference in these variables between the two groups.
3. After treatment with 40 μg of 25-(OH)D3 daily for 7 days, there was a significant increase in plasma 25-(OH)D and 1,25-(OH)2D in both groups of women, but radio-calcium absorption increased significantly only in the group without vertebral fractures.
4. Elderly women with vertebral fractures have malabsorption of calcium which is resistant to the action of vitamin D metabolites at concentrations which correct calcium malabsorption in elderly women without vertebral fractures.
Prostaglandins Cause An Increase in Serum Acute-Phase Proteins in Man, Which is Diminished in Systemic Sclerosis
Authors: Whicher J. T. , Bell A. M. , Martin M. F. R. , Marshall L. A. , Dieppe P. A. 
Published: August 2015

1. The prostaglandin E1 increases the plasma concentration of acute-phase proteins in man and decreases the concentration of certain carrier proteins.
2. This response is greatly diminished in patients with systemic sclerosis, a chronic inflammatory disease leading to fibrosis.
3. These findings pose new questions about the mediation of the acute-phase response and its role in controlling the inflammatory process.
Baroreflex Setting and Sensitivity after Acute and Chronic Nicardipine Therapy
Authors: Young M. A. , Watson R. D. S. , Littler W. A. 
Published: August 2015

1. Intra-arterial pressure, baroreflex sensitivity and the baroreflex set point were measured in eight patients with essential hypertension during a control period and then after acute treatment (2 h after a 30 mg oral dose) and after chronic treatment (at least 2 months) with nicardipine hydrochloride, a calcium channel antagonist.
2. Mean intra-arterial blood pressure fell after the acute treatment from 130 ± 14 (sd) control to 118 ± 11 mmHg, P&lt;0.05, and after chronic treatment to 112 ± 19 mmHg, P&lt;0.05. Heart rate increased from 72 ± 11 control to 81 ± 16 beats/min, P&lt;0.05, during acute treatment indicating activation of the baroreflex control mechanism, but returned to control values with chronic treatment (72 ± 11 control vs 69 ± 9 beats/min chronic), indicating a significant shift to the left of the baroreflex set point. There was no change in baroreflex sensitivity after either acute or chronic treatment (control 4.7, acute 4.3, chronic 5.1 ms/mmHg, P not significant for all values).
3. Nicardipine significantly reduces mean intraarterial pressure both acutely and chronically; the latter is associated with a return of the heart rate to control values due to resetting of the baroreflex control mechanism.
Captopril Enhances Vascular and Adrenal Responsiveness to Angiotensin II in Essential Hypertension
Authors: Koletsky Richard J. , Gordon Murray B. , Leboff Meryl S. , Moore Thomas J. , Dluhy Robert G. , Hollenberg Norman K. , Williams Gordon H. 
Published: August 2015

1. The converting-enzyme inhibitor captopril (25–50 mg orally every 6 h for 66 h) was used to dissociate the circulating levels of angiotensin II (ANG II) from changes in sodium balance in 11 patients with normal renin essential hypertension on 10 mmol of sodium/day intake. Pressor, renal vascular and adrenal responses to graded infusions of ANG II (0.3, 1 and 3 pmol kg−1 min−1) were measured before and after captopril administration. Systemic vascular responses were assessed by measuring diastolic blood presusre (DBP), renovascular responses by measuring p-aminohippurate (PAH) clearance and adrenal responses by measuring plasma aldosterone.
2. After receiving captopril for 66 h the hypertensive subjects showed a significantly (P&lt;0.004) enhanced blood pressure response to the infused ANG II but not to noradrenaline when compared with the response before captopril. ANG II (3 pmol kg−1 min−1) also produced a significantly (P&lt;0.03) greater reduction in PAH clearance after (−194 ± 40 ml/min) compared with before (−104 ± 15 ml/min) captopril. These results suggest that the responsiveness to ANG II in these two target tissues is determined by the circulating ANG II level.
3. In the adrenal gland the aldosterone responses to ANG II also were significantly greater after (P &lt; 0.01) than before captopril (increment at 3 pmol kg−1 min−1: 660 ± 88 vs 381 ± 94 pmol/l). These results are in distinct contrast with the responses previously reported for normotensive subjects and support the hypothesis that the regulation of aldosterone secretion is altered in subjects with essential hypertension.
A Passive Sodium Transport Inhibitory Factor (Inhibitin) Released from Leukaemic Promyelocytes in Culture
Authors: Morgan Kevin , Mir M. Afzal 
Published: August 2015

1. Previous studies have shown that myeloid leukaemic blast cells contain a heat stable factor which inhibits bidirectional sodium transport in normal erythrocytes. This study was undertaken to establish whether leukaemic promyelocytes in culture secrete this factor.
2. Two cell-lines of leukaemic promyelocytes (HL-60 and JR) were grown and culture media from both reduced significantly the ouabain-insensitive sodium efflux rate constant, whereas conditioned culture medium (incubated like the cells in culture) had no inhibitory effect.
3. Promyelocyte extract reduced significantly (P &lt; 0.01) the total sodium efflux rate constant from 0.393 ± 0.030 (sd) to 0.311 ± 0.060, and ouabain-insensitive efflux rate constant from 0.131 ± 0.008 to 0.079 ± 0.009 (P&lt;0.001).
4. The inhibitory factor was heat stable (80°C for 30 min) and it inhibited sodium efflux through a pathway which was not inhibited by ouabain or frusemide.
5. These studies suggest that leukaemic promyelocytes secrete the previously identified passive sodium transport inhibitory factor.
The Effects of Platelet-Derived Contractile Agents on Human Digital Arteries
Authors: Moulds R. F. W. , Iwanov V. , Medcalf R. L. 
Published: August 2015

1. The contractile responses of spiral strips of human digital arteries to samples of a suspension of human platelets aggregated by thrombin have been studied at different time intervals after aggregation.
2. Platelets added to the arterial strips 1 min after aggregation of the platelets produced contractile responses which were significantly greater than those produced by corresponding platelets added 20 min after aggregation.
3. When platelets were aggregated in the presence of indomethacin or the thromboxane synthetase antagonist 1-benzylimidazole, contractile responses produced by the platelets 1 min after aggregation were significantly reduced. They were then not significantly different from those produced by addition of the aliquots 20 min after aggregation, which were unaffected.
4. Pretreatment of the arteries with the serotonin antagonist ketanserin nearly abolished the contractile responses produced by addition of the platelets 20 min after aggregation, and significantly reduced those produced by addition of the platelets 1 min after aggregation.
5. Ketanserin did not affect the contractile responses of the arteries to potassium chloride, prostaglandin F2α, or the endoperoxide analogue U-46619, but antagonized the contractile effects of exogenous serotonin.
6. Combination of pretreatment of the arteries with ketanserin and aggregation of the platelets in indomethacin or 1-benzylimidazole virtually abolished contractile responses to platelets added both 1 min and 20 min after aggregation.
7. Tensions developed to different dilutions of platelets added 1 min after aggregation to arteries pretreated with ketanserin were not significantly different from those obtained to the same dilutions added 20 min after aggregation to arteries not pretreated with ketanserin.
8. It is concluded that there are two components to the contractile responses of human blood vessels produced by the aggregation of human platelets. One is labile, not produced when aggregation occurs in indomethacin or 1-benzylimidazole and is probably produced by thromboxane A2. The other is stable, markedly reduced by ketanserin, and probably produced by serotonin. Each of the components makes an approximately equal contribution to the contractures of human blood vessels produced by platelet aggregation.
9. It is also concluded that serotonin antagonists, in combination with a thromboxane synthetase inhibitor, may be of therapeutic benefit in clinical syndromes possibly mediated by platelet aggregation, such as cerebral transient ischaemic attacks and coronary spasm.
Effect of Unclipping on Pressor Responses in Rats with Renovascular Hypertension
Authors: Bing Robert F. , Swales John D. , Taverner David , Thurston Herbert 
Published: August 2015

1. Pressor responses to angiotensin II and noradrenaline have been examined in two models of renovascular hypertension (two-kidney one-clip and one-kidney one-clip) before and 24 h after removal of the renal artery clip to examine the possible role of pressor hyper-responsiveness in the maintenance of hypertension. Early and chronic hypertension was studied to assess the part played by progressive structural hypertrophy.
2. Plasma renin concentration was elevated in early two-kidney hypertensive rats, whereas it was similar to that in age-matched normal rats in early one-kidney and chronic two-kidney hypertensive rats. Twenty-four hours after unclipping plasma renin concentration was the same in all groups. Unclipping restored blood pressure to normal levels by 24 h, whereas sham-operated animals remained hypertensive.
3. Angiotensin II responses in both early and chronic two-kidney one-clip hypertensive rats were lower than in age-matched normal rats. In unclipped rats responses were similar to those in normals. One-kidney hypertensive rats had similar angiotensin II responses to normal rats and there was no change with unclipping. Blockade of endogenous angiotensin II production by converting enzyme inhibition resulted in similar angiotensin II responses in hypertensive and unclipped groups.
4. In normal rats, angiotensin II responses were inversely related to plasma renin concentration (r = −0.47, P&lt;0.001). Angiotensin II responses in hypertensive and unclipped rats were found to show a similar relationship to plasma renin concentration as normal rats.
5. Noradrenaline responses in hypertensive rats were similar to those in age-matched normals and there was no significant change with unclipping. In normal rats there was no relationship between noradrenaline responses and plasma renin concentration (r = −0.11, P&lt;0.5).
6. These results emphasize the importance of the activity of endogenous renin-angiotensin in determining angiotensin II responses in vivo. It is concluded that neither the maintenance of hypertension nor the fall in blood pressure produced by removal of the renal artery clip in renovascular hypertension is due to changes in responsiveness to angiotensin II.
Bilirubin Content and 4-Nitrophenol Glucuronosyltransferase Activity in Gunn Rat Liver
Authors: Celier Chantal , Foliot Armelle 
Published: August 2015

1. The purpose of this study was to determine whether the hepatic content of bilirubin could influence liver 4-nitrophenolglucuronosyltransferase (4-NP-GT) in the Gunn rat.
2. In animals fed on a 45% lipid diet, compared with rats fed on a normal lipid diet (3%), the bilirubin content of the hepatic microsomal fraction decreased and the bilirubin/protein ratio was reduced. 4-NP-GT activities were comparable in both groups.
3. Administration of clofibrate to Gunn rats greatly enhanced the bilirubin content of liver microsomal fraction. Since this treatment raised the microsomal protein content, the bilirubin/protein ratio was not modified. No significant change in 4-NP-GT was noted.
4. After bilirubin perfusion in Gunn and Wistar rats, no change was observed in hepatic monooxygenase activities or in 4-NP-GT, although the bilirubin/protein ratio was dramatically increased in the microsomal fraction.
5. From these results the low activity of liver 4-NP-GT in Gunn rats does not seem directly related to the hepatic content of bilirubin.
Radionuclide Demonstration of Ventilatory Abnormalities in Mild Asthma
Authors: Agnew J. E. , Bateman J. R. M. , Pavia D. , Clarke S. W. 
Published: August 2015

1. The distribution of 5 μm 99mTc aerosol particles deposited in the lungs was compared with that of 81mKr gas in 20 asthmatic subjects (FEV1.0≥75% predicted) whose asthma was mild or in remission. Sixteen normal non-smokers and 14 ‘normal’ cigarette smokers were studied as control subjects.
2. Radioaerosol lung penetration in the ‘normal’ smokers was the same as in the normal non-smokers but was reduced in the asthmatic subjects.
3. Radioaerosol penetrated better than 81mKr to the lung apices of normal non-smokers and asthmatic subjects; it penetrated better than 81mKr to the lung bases of the asthmatic subjects.
4. Uneven distribution of aerosol relative to 81mKr related strongly to maximal mid-expiratory flow rate (MMFR) in the asthmatic subjects.
5. Aerosol deposition abnormalities in symptom-free asthmatic subjects may reflect basal airways closure at functional residual capacity and abnormal patterns of lung filling.
Exchangeable Sodium in Goldblatt One-Kidney One-Clip Hypertension in the Rat
Authors: McAreavey D. , Brown W. B. , Murray G. D. , Robertson J. I. S. 
Published: August 2015

1. Exchangeable sodium (NaE), plasma active renin concentration and blood pressure were measured in rats with a sole remaining kidney before and after the development of hypertension induced by clipping of the single renal artery and again after unclipping.
2. Control observations were made in sham-clipped and sham-unclipped uninephrectomized rats.
3. Renal artery clipping caused hypertension and expansion of NaE, the latter being sustained throughout the 6 weeks during which the renal artery was constricted.
4. Hypertension in the clipped rats was progressive over 6 weeks, whereas the expansion of NaE was not; thus the two measurements were not significantly correlated.
5. Two rats which remained normotensive after clipping did not show expansion of NaE.
6. Plasma active renin was elevated in comparison with the sham-clipped controls on the day after clipping, but not thereafter.
7. Unclipping in hypertensive rats was followed by a return of NaE and blood pressure to control values.
8. Both the sustained expansion of NaE and the transient rise in active renin probably contribute to the development of hypertension in this model, but neither alone nor together do they provide a full satisfactory explanation.
Studies of Salivary Flow in Borderline Hypertension: Effects of Drugs Acting on Structures Innervated by the Autonomic Nervous System
Authors: Van Hooff M. , Van Baak M. A. , Schols M. , Rahn K. H. 
Published: August 2015

1. Salivary flow and the influence of drugs on this were studied in subjects with borderline hypertension and in normotensive subjects.
2. Saliva production at rest was lower in borderline hypertensive subjects than in normotensive subjects. Plasma catecholamine levels were similar in both groups of subjects studied.
3. Intravenous injections of propranolol and phentolamine did not enhance saliva secretion in the borderline hypertensive group, whereas atropine caused the secretion to decrease in both groups. Intravenous infusions of neostigmine led to a dose-dependent increase of salivary flow. The dose-response curve for the stimulating effect of neostigmine on saliva production was shifted to the right in borderline hypertensive as compared with normotensive subjects.
4. The results of the study support the assumption that in subjects with borderline hypertension parasympathetic influence on the salivary glands is reduced.