bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ventilatory Pattern and Drive after Acute Myocardial Infarction
Authors: Clarke H. , Dhingra S. , Anthonisen N. R. 
Published: August 2015

1. In 18 patients with acute myocardial infarction, we measured ventilation, frequency, inspiratory duration and the pressure at the mouth 0.1 s after the onset of inspiration against an occluded airway; mean inspiratory flow and the fraction of the breathing cycle devoted to inspiration were calculated. Measurements were made on 2–3 consecutive days soon after admission and repeated 4–10 days after admission.
2. Eight patients showed no clinical evidence of left heart failure at any time; in these patients no changes in breathing pattern, ventilation or occlusion pressure were observed.
3. Ten patients were in heart failure, as judged by the presence of râles and/or hypoxaemia on day 1 of the study, and all had recovered on the last day. When in failure these patients demonstrated increased minute ventilation, occlusion pressure was increased more than was mean inspiratory flow and their breathing pattern was altered. Tidal volume was similar to that in patients without failure and did not change with time, but frequency was initially high and fell as recovery from failure occurred. The duration of inspiration was decreased during failure, so mean inspiratory flow was increased. The fraction of the breathing cycle devoted to inspiration was constant and similar to that in patients without failure.
4. While in failure no patients were acidotic and not all patients were hypoxaemic; administration of oxygen did not influence results in two patients during failure.
5. These results indicate that clinically detectable pulmonary oedema is associated with increased ventilatory drive, which cannot be explained on the basis of hypoxaemia or hypercapnia. The observed changes in breathing pattern were probably due at least in part to vagal reflexes, and these may have contributed to the increase in drive.
Renin Release during Head-up Tilt Occurs Independently of Sympathetic Nervous Activity in Tetraplegic Man
Authors: Mathias C. J. , Christensen N. J. , Frankel H. L. , Peart W. S. 
Published: August 2015

1. The role of the sympathetic nervous system in the release of renin during head-up tilt has been studied in five normal subjects and in four tetraplegic patients with cervical spinal-cord transection above the sympathetic outflow. Blood pressure, heart rate and concentrations of plasma noradrenaline, plasma adrenaline and plasma renin activity were measured during head-up tilt to 45° before and after acute β-adrenoreceptor blockade with intravenous propranolol.
2. In the normal subjects there were minimal changes in blood pressure during head-up tilt and there was a rise in both plasma noradrenaline concentration and plasma renin activity. After propranolol values of plasma renin activity at rest fell with little change occurring during head-up tilt.
3. In the tetraplegic patients there was a substantial fall in blood pressure during head-up tilt. Concentrations of plasma noradrenaline and adrenaline did not change but there was a marked increase in plasma renin activity. Values of plasma renin activity both at rest and during head-up tilt were unaffected by propranolol.
4. We conclude that in tetraplegic patients renin release during head-up tilt may occur independently of sympathetic nervous activity and is probably largely dependent on activation of renal vascular receptors.
Propionate Enhancement of Acetoacetate Oxidation in Perfused Rat Hearts
Authors: Revsin-Lanier Betty , Lebowitz Joyce , Morrow Grant 
Published: August 2015

1. In isolated perfused rat hearts, acetoacetate oxidation was significantly enhanced by propionate.
2. No enhancement of acetoacetate oxidation could be observed in vitamin B12-deficient rat hearts when propionate was present.
3. Although the mechanisms of enhancement are not clear, ketone clearance is enhanced by propionate and may provide an insight into the therapy of certain diseases characterized by ketosis.
Renin Precursor from Mouse Kidney Identified by Cell-Free Translation of Messenger RNA
Authors: Poulsen K. , Vuust J. , Lund T. 
Published: August 2015

1. The biosynthetic precursor of renin (pre-prorenin) from mouse kidney is a single chain polypeptide with a molecular weight of 50 000.
2. This is the same value as previously found for mouse submaxillary gland pre-prorenin.
3. Mouse kidney pre-prorenin (mol. wt. 50 000) is larger than the enzymatically active renin (mol. wt. 40 000).
Regional Lung Function in Bilateral Diaphragmatic Paralysis
Authors: Amis T. C. , Ciofetta G. , Hughes J. M. B. , Loh L. 
Published: August 2015

1. The distribution of regional function in the lungs of six patients with bilateral diaphragmatic paralysis was investigated by continuous inhalation and infusion of the radioactive gases 81mKr and 85mKr during tidal breathing.
2. In the supine and right lateral decubitus postures the vertical distribution of ventilation per unit alveolar volume was less in the dependent zones, the reverse of that found in normal subjects. In the upright posture ventilation was slightly decreased at the lung base. Perfusion per unit alveolar volume was more uniformly distributed than normally in the upright posture, and decreased from superior to inferior in the supine posture. In the lateral decubitus posture, perfusion of the lower lung was greater than that of the upper. Ventilation/perfusion ratios were more uniformly distributed in the patients than in normal subjects, except in the right lateral decubitus posture.
3. Alterations in the distribution of ventilation may be explained in terms of the altered mechanical interaction of chest wall, mediastinal and abdominal contents, with selective use of intercostal and accessory muscles. The effects on the distribution of blood flow are probably related to the low end-expiratory lung volume.
Effect of Moderate Salt Restriction and High Potassium Intake on Pressor Hormones, Response to Noradrenaline and Baroreceptor Function in Man
Authors: Skrabal F. , Aubouck J. , Hourtnagl H. , Braunsteiner H. 
Published: August 2015

1. Twenty-one normotensive subjects were studied to assess any possible benefits of moderate salt restriction and of high potassium intake in the prevention of hypertension in man.
2. The effects of salt reduction from 200 to 50 mmol/day and/or of an increase of potassium intake from 80 to 200 mmol/day over a 2 week period, on blood pressure, plasma noradrenaline, adrenaline, vasopressin, renin and aldosterone, were measured both at rest and after mental stress. The effects of graded infusion of noradrenaline on blood pressure and heart rate were also studied.
3. Salt restriction lessened the increase of blood pressure during noradrenaline infusion; the combination with high potassium intake also reduced the pressure rise after mental stress. There were no major changes in plasma levels of vasopressin and adrenaline. Plasma noradrenaline increased during the low sodium diet.
4. High potassium intake improved baroreceptor function as revealed by the greater decrease in heart rate for a given rise in pressure after noradrenaline infusion.
5. The results of this study are compatible with a protective effect of a practicable low sodium/high potassium diet on the development of human hypertension.
Haemodynamics of Renoprival Hypertension in Man: Studies during Graded Fluid Withdrawal
Authors: Man in 'T Veld A. J. , Schalekamp M. A. D. H. 
Published: August 2015

1. Frequent measurements of arterial pressure, cardiac output, heart rate and body weight were carried out in three hypertensive anephric subjects during the reversal of hypertension by carefully controlled stepwise fluid withdrawal over a period of 24 days.
2. The initial 5% decrease of body weight was associated with decrements of arterial pressure and total peripheral resistance of 15 and 35% respectively, whereas cardiac output had risen by 25%. After a further decrease in body weight by 5%, arterial pressure was lowered another 15% without a change in total peripheral resistance, and cardiac output had returned to base line.
3. These data do not support the concept that whole-body autoregulation is an important factor in the pathogenesis of renoprival hypertension.
Altered Cardiac β-adrenoreceptors in Spontaneously Hypertensive Rats Receiving Salt Excess
Authors: MacPhee A. A. , Blakesley H. L. , Graci Karen A. , Frohlich E. D. , Cole F. E. 
Published: August 2015

1. Altered adrenergic responsiveness of hearts and blood vessels occurs in both experimental and clinical hypertension.
2. Since salt excess aggravates both types of hypertension, we investigated β-adrenoreceptor properties in the hearts of spontaneously hypertensive and normotensive rats drinking 1% NaCl or tap water for 3 weeks.
3. Sodium loading increased heart weight in both spontaneously hypertensive and normotensive rats.
4. In spontaneously hypertensive rats excess salt attenuated the age-related decrease in β-adrenoreceptor number observed in spontaneously hypertensive and normotensive rats drinking tap water and in normotensive rats drinking 1% NaCl.
5. Unlike the normotensive rats, which did not show a relationship between β-adrenoreceptor number and blood pressure, spontaneously hypertensive rats on tap water and 1% NaCl showed a significant negative logarithmic relationship between these two variables. These data provide further evidence implicating sodium excess as an aggravating factor in this model of experimental hypertension.
Effects of Variations in Sodium Intake on the Acute Vasodepressor Response to Kininase II Inhibition in Rats with Mild Two-Kidney, One-Clip Hypertension
Authors: Kushiro T. , Lee T. C. , Girolami J. P. , Gassia J. P. , Maxwell M. H. 
Published: August 2015

1. Unilateral renal artery constriction in rats maintained on a sodium-deplete, but not sodium-replete, diet induced an augmented acute vasodepressor response to kininase II inhibition produced by an intravenous injection of the dipeptidyl carboxypeptidase inhibitor captopril (250 μg) during continuous saralasin-induced angiotensin II blockade (10 μg/min). Dietary sodium restriction alone in sham-operated rats had no effect.
2. Acute bilateral adrenalectomy (18-24 h) did not preclude the demonstration of an augmented response to kininase II inhibition in sodium-depleted rats with benign two-kidney, one-clip hypertension. Neither did chronic administration of deoxycorticosterone acetate in intact rats elicit an augmented response.
3. The augmented acute vasodepressor response to kininase II inhibition in sodium-depleted rats with benign two-kidney, one-clip hypertension is probably due to bradykinin potentiation and secondary to an increased activity of the kallikrein-kinin system. The mechanism responsible for this apparent increase is not known, but neither hyperangiotensinemia nor hyperaldosteronism seems to play a role.
Vascular Sodium—Potassium Pump Activity in Various Models of Experimental Hypertension
Authors: Pamnani M. B. , Clough D. L. , Huot S. J. , Haddy F. J. 
Published: August 2015

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension.
2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension.
3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.
Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin
Authors: Rockhold R. W. , Crofton J. T. , Share L. 
Published: August 2015

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection.
2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure.
3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats.
4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin.
5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.
Determination of Noradrenaline Uptake, Spillover to Plasma and Plasma Concentration in Patients with Essential Hypertension
Authors: Esler M. , Jackman G. , Leonard P. , Bobik A. , Skews Helen , Jennings G. , Kelleher Dianne , Korner P. 
Published: August 2015

1. The rates of entry of noradrenaline to plasma and of removal of noradrenaline from plasma, and plasma noradrenaline concentration, were determined in normal subjects and in patients with essential hypertension. Neuronal uptake of noradrenaline was assessed from the plasma tritiated noradrenaline disappearance curve, after infusion to steady state.
2. Noradrenaline disappearance was biexponential. Rapid removal was dependent on neuronal uptake, being slowed if neuronal noradrenaline uptake was reduced, either by desipramine in normal subjects, or in patients with sympathetic nerve dysfunction (autonomic insufficiency).
3. In 10 of 41 hypertensive patients the t1 1/2 similarly was prolonged, presumptive evidence of a defect in neuronal noradrenaline uptake. Endogenous noradrenaline escaping uptake after release, and spilling over into plasma, and plasma noradrenaline concentration, were increased in these patients.
4. Defective neuronal uptake of noradrenaline, by exposing adrenoreceptors to high local transmitter concentration, may be important in the pathogenesis of essential hypertension in some patients.
Is Arterial Media Hypertrophy in Spontaneously Hypertensive Rats a Consequence of or a Cause for Hypertension?
Authors: Henrichs K. J. , Unger T.H. , Berecek K. H. , Ganten D. 
Published: August 2015

1. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. This study was undertaken to examine the possiblity that structural changes in the arterial bed are genetically determined and may be causative factors in the development of high blood pressure in the spontaneously hypertensive rat.
2. The wall dimensions of aorta, renal artery and intrarenal arteries down to a distended diameter of 35 μm were studied: (a) in 14-week-old spontaneously hypertensive rats; (b) in age- and sex-matched spontaneously hypertensive rats which had been treated with captopril for two generations and had been normotensive during their complete life span; (c) in normotensive Wistar-Kyoto control rats.
3. Cross-sectional areas of the media were increased in the hypertensive rats in comparison with ‘normotensive spontaneously hypertensive rats’ and Wistar-Kyoto rats. Increased numbers of smooth muscle cells were found in the major arteries of hypertensive animals.
4. These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats.
Cardiac Contractile Reserve in Spontaneously Hypertensive Rats
Authors: Saragoca M. A. , Tarazi R. C. 
Published: August 2015

1. In response to graded infusions of isoprenaline, adult spontaneously hypertensive rats (20-24 weeks old) showed diminished responses of left ventricular contractile indices, diminished chronotropic responses and impairment of left ventricular relaxation rate as compared with matched Kyoto-Wistar rats.
2. These findings suggest reduced capacity to increase contractility in response to stress.
Myocardial Infarction in Experimental Hypertension in Rats: Mechanism of the Reduction in Blood Pressure
Authors: Fletcher P. J. , Pfeffer Janice M. , Pfeffer M. A. , Braunwald E. 
Published: August 2015

1. Haemodynamic changes during graded methoxamine infusion have been measured in 16 spontaneously hypertensive rats with healed myocardial infarction produced by left coronary artery ligation and in 15 hypertensive rats without infarction.
2. Arterial pressure of the hypertensive rats was reduced to levels within the normotensive range in animals with moderate and large myocardial infarctions.
3. The peripheral vascular response to methoxamine was similar in rats with and without infarction.
4. The reduction in blood pressure resulted from a combination of lower heart rate and inability to maintain stroke volume at hypertensive pressures.
Left/Right Ventricular Weight Ratio: An Estimate of ‘Cardiac Adaptation to Hypertension’
Authors: Hallbauck-Nordlander Margareta 
Published: August 2015

1. Left and right ventricular weights were determined in newborn, 6, 15 and 28 week-old spontaneously hypertensive and normotensive control rats.
2. Left and right ventricles were heavier in all spontaneously hypertensive rats than in age-matched control rats, but the left/right ventricular weight ratio was increased only in 15 and 28 week-old spontaneously hypertensive rats.
3. If the cardiomegaly in newborn spontaneously hypertensive rats, in which the two ventricles have worked in parallel until birth, is an adaptation to hypertension in utero, left ventricular weight would rapidly increase after birth as the left ventricle alone is then exposed to an increased pressure. As left/right ventricular weight ratio was not increased in 6 week-old spontaneously hypertensive rats, factors other than hypertension may stimulate cardiac growth in the foetal spontaneously hypertensive rat.
4. This implies an initial structural ‘resetting’ of the cardiovascular dimensions in spontaneously hypertensive rats and that true pressure-dependent adaptation further potentiates these alterations in cardiovascular structure once hypertension is initiated.
Effect of Blood Pressure Control on Left Ventricular Hypertrophy in Patients with Essential Hypertension
Authors: Dunn F. G. , Bastian B. , Lawrie T. D. V. , Lorimer A. R. 
Published: August 2015

1. Changes in left ventricular structure and function were assessed by echocardiography in 22 patients before and after 9 months blood pressure control.
2. Nine patients had normal baseline echocardiograms (group 1) and 13 had echocardiographic evidence of left ventricular hypertrophy (group 2).
3. Group 2 patients demonstrated significant reductions in posterior wall thickness (P&lt;0.01), septal wall thickness (P&lt;0.025) and left ventricular mass (P&lt;0.005). Only six of the 13 patients showed a reduction of ≥3 mm in posterior wall thickness. The remainder showed no alteration or only a slight non-significant reduction.
4. The regression of voltage in some patients but not in others did not appear to be related to initial blood pressure, the extent of the fall in blood pressure or duration of follow-up. It was not possible to say whether any specific therapy was beneficial to regression since most of the patients were on multiple therapy.
Hydrallazine: Mode of Action at the Neuroarterial Junction
Authors: Chevillard C. , Saiag B. , Worcel M. 
Published: August 2015

1. Hydrallazine relaxes the rat tail artery by a direct action on vascular smooth muscle cells, which appears to be modulated by the action of sympathetic nerve terminals.
2. There is a gradient of response to hydrallazine in arteries from normotensive Wistar rats, the proximal segments being poorly responsive. This gradient disappears after denervation with 6-hydroxydopamine in vitro.
3. Exogenously added purines inhibit noncompetitively the vasodilator response to hydrallazine in denervated segments from normotensive Wistar rats. Their order of potency is 2-Cl-adenosine &gt; adenosine &gt; ATP &gt; inosine.
4. The effect of hydrallazine in innervated, poorly responsive segments is greatly potentiated by theophylline (50 μmol/l) and propranolol (5 μmol/l). These results, together with the effect of denervation, suggest that there are endogenous purines leaking from the nerve terminals under our experimental conditions.
5. Hydrallazine produces a marked inhibition of stimulus-induced contraction and 3H release after [3H]noradrenaline loading. The mechanism of this prejunctional action appears to be different from the mechanism of the postjunctional effect.
Comparison of Ventilation/Perfusion Lung-Imaging and Dead-Space Measurements in Airway Disease
Authors: Noble M. I. M. , Langley F. , Buckman M. , Vernon P. , Seed A. , Jewkes R. , Bisdee A. , Cumming G. 
Published: August 2015

1. Nineteen patients (three normal subjects, and 16 patients with chronic airway disease) were investigated with radionuclide lung-imaging and pulmonary function tests.
2. There was a statistically significant correlation between the ratio of residual volume to total lung capacity and alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation (an index of gas mixing inefficiency); rS = 0.54, P &lt; 0.05.
3. There were statistically significant associations between an abnormal ventilation or perfusion radionuclide lung image and (a) the ratio of residual volume to total lung capacity and (b) the alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation.
4. The radionuclide counts from the posterior images were normalized for lung size and injected dose; perfusion counts were then subtracted from ventilation counts at locations from the top to the bottom of the lungs.
5. There was a statistically significant association between low ventilation minus perfusion areas and arterial hypoxia.
6. There was a statistically significant association between high ventilation minus perfusion areas and an increased alveolar dead-space ventilation for carbon dioxide as a percentage of alveolar ventilation.
The Effect of Prolonged Administration of Propranolol and Timolol on the Growth and the Heart of Growing Rabbits
Authors: Evemy K. L. , Cummins P. , Littler W. A. 
Published: August 2015

1. The effect of prolonged administration of β-adrenoreceptor-blocking agents was studied in growing rabbits. Equivalent doses of propranolol and timolol were given parenterally for 8 weeks.
2. Animals given propranolol had a significantly lower heart rate than that in the controls. After subcutaneous injection, plasma propranolol levels were twice those obtained after intraperitoneal injection.
3. Growth rate of animals given propranolol intraperitoneally was significantly less than controls, whereas animals given propranolol subcutaneously or timolol intraperitoneally grew normally. Reduced growth rate was associated with reduced food intake and was not related to the β-adrenoreceptor-blocking activity of the drugs.
4. At the end of the experiment the heart and other organs were examined. β-Adrenoreceptor blockade produced no significant changes in ventricular size or water content, and no significant changes in ultrastructure were found.