bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ambulatory ECG Recording in Patients Referred because of Syncope or Dizziness
Authors: Kala Risto , Viitasalo Matti T. , Toivonen Lauri , Eisalo Antti 
Published: August 2010

ABSTRACT. Data are presented on patients referred for ambulatory ECG recording because of syncope or dizziness during a 2‐year period. Of the 272 consecutive patients subjected to the recording, 107 (39.3%) had syncope or dizziness as the main indication for referral. Sixteen of these patients (14.9%) experienced the presenting symptom during the recording, and in 8 (50%) of these the simultaneous ECG finding was interpreted as causative.In patients who were symptom‐free during the recording, sinus arrests exceeding 2.5 seconds seemed to be a valuable finding to support the cardiac aetiology of the syncopal symptoms, whereas the diagnostic value of second degree AV block with either Wenckebach or Mobitz II like patterns, as such, and of ventricular tachycardia remained mostly unsettled.
CHANGES IN INTRAERYTHROCYTE CONTENT AND TRANSMEMBRANE FLUXES OF SODIUM DURING SALT LOADING IN SUBJECTS WITH AND WITHOUT FAMILY HISTORY OF HYPERTENSION
Authors: Herlitz Hans , Gudmundsson Ottar , Jonsson Olof , Nauclér Jacob , Berglund Göran 
Published: August 2010

ABSTRACT. We studied 17 young normotensive men with family history of hypertension (H) in two generations (father and grandfather) and 17 age matched control subjects (C) with respect to intraerythrocyte sodium (IeNa), sodium influx, and rate of sodium efflux. The investigation was done during ordinary salt intake and after four week's salt load.H had a significantly higher IeNa (9.5 ± 0.4 mmol/l) compared to C (8.2 ± 0.3 mmol/l), p < 0.01. After salt loading H decreased significantly to 8.1 ± 0.3 mmol/l while C did not change significantly (7.6 ± 0.3 mmol/l). There was no significant difference between H and C in Na influx either on normal or on high salt intake. The rate constant for Na efflux was significantly lower on normal salt intake in H (0.0038 ± 0.0003 vs 0.0050 ± 0.0004 min, p < 0.05). High salt intake increased the efflux rate constant significantly in H (0.0048 ± 0.0003 min‐1, p < 0.05), while control subjects showed no difference (0.0053 ± 0.0004 min‐1) compared to pre‐salt conditions.Our results suggest that young men with heredity for hypertension have a higher intraerythrocyte Na‐content secondary to a lower rate of Na efflux. The Na influx did not differ between the two groups probably indicating an unchanged permeability for sodium in subjects with a family history of hypertension.
On the Mechanism of Action of Calcium Antagonists
Authors: Andersson K.‐E. , Högestätt E.D. 
Published: August 2010

SummaryA short review is given of possible mechanisms of action of the organic “calcium antagonists”. Calcium antagonists comprise a chemically heterogenous group of drugs, and the term may be used to denote agents that inhibit Ca2+‐dependent processes or regulatory mechanisms without acting at other sites. Such drugs may be subdivided into those that decrease the availability of Ca2+ to the myoplasm, and those that decrease the cellular effects of Ca2+ without lowering the intracellular Ca2+ concentration. Accordingly, calcium channel blockers, such as verapamil, nifedipine, and diltiazem, form a subgroup of calcium availability inhibitors, as they block influx of extracellular calcium through ion selective channels in the membrane both in cardiac and smooth muscle. However, it cannot be excluded that some of these drugs, particularly in smooth muscle, may have additional sites of action, which must be taken into consideration when they are used as investigational tools.
Influence of Verapamil on Glucose Tolerance
Authors: Röjdmark Sven , Andersson Dan E.H. 
Published: August 2010

SummaryVerapamil has previously been found to inhibit insulin release from pancreatic β‐cells in laboratory animals. In our department, however, both oral pretreatment with verapamil for one week and a 3‐hour iv infusion of the drug improved the tolerance to oral glucose in type II diabetics without affecting insulin release. It failed, however, to potentiate the hypoglyemic effect of oral glibenclamide therapy in patients with type II diabetes. Since iv infusion of verapamil left the portal vein glucose response to glucose ingestion unaffected in normoglycaemic patients (being portal vein catheterised for diagnostic purposes), it seems unlikely that the hypoglyceamic effect of verapamil could have been due to reduced glucose absorption from the gut. More likely is that verapamil, in the diabetic patients, influenced metabolic processes inside the hepatocytes that are of importance for glucose homeostasis.In‐vitro experiments have shown that calcium affects factors of importance for the glucose metabolism. Accordingly, calcium triggers the stimulus‐secretion coupling process which leads to insulin release from the pancreatic β‐cells (1). Calcium also tightens cell membranes, thereby decreasing their permeability to various substances, including glucose (2). Finally, calcium mediates cellular responses to glucagon stimulation (3,4) and thus affects the hepatic glucose output. Calcium apparently influences glucose metabolism by several pathways and different overall effects on the blood glucose concentration may be forthcoming depending on which of these pathways is the dominating one.In view of these well‐documented in‐vitro effects of calcium on some of the metabolic processes which determine the glucose tolerance, it is surprising to find that relatively few clinical studies have been carried out to investigate whether calcium antagonists influence glucose tolerance in man. Although a few such studies, dealing with the effect of nifedipine (5,6) and verapamil (7,8,9,10) on human glucose tolerance have been performed recently, the result obtained in these investigations have been highly conflicting. Our intention has therefore been to elucidate how oral and iv administration of verapamil affects glucose tolerance not only in normoglycaemic subjects, but also in patients with untreated, and sulfonylurea‐treated type II diabetes.
Verapamil or Propranolol in the Treatment of Stable Angina Pectoris of Effort
Authors: Sigurd Bjarne , Fischer Jørgen 
Published: August 2010

SummaryIn a double blind cross‐over study the effect of verapamil (Isoptin) 360 mg/d and propranolol 180 mg/d was evaluated in patients with stable angina of effort. The results of verapamil and propranolol treatment were compared to a single blind placebo period of 2 weeks.Both verapamil and propranolol caused a significant reduction in nitroglycerin consumption, days with angina pectoris and in severe angina attacks as compared to placebo. A 50% reduction in angina pectoris attacks and/or nitroglycerin consumption compared to placebo was demonstrated in thirteen of eighteen patients during verapamil treatment (P < 0.01) and in seven of seventeen patients during propranolol treatment (P > 0.05). Of sixteen patients completing both treatment periods, ten were improved both on verapamil and propranolol, three on verapamil only, one on propranolol only, one was unchanged and one deteriorated on verapamil and propranolol. During exercise, maximum exercise capacity was increased during verapamil as compared to placebo (P < 0.01) and propranolol (P < 0.02). Maximum exercise capacity was not increased after propranolol as compared to placebo.These findings, that verapamil is at least as effective as propranolol in the treatment of angina of effort, are in accordance with other reported series.
Verapamil and Propranolol: A Comparison of Two Antihypertensive Agents
Authors: Leonetti G. , Pasotti C. , Ferrari G.P. , Zanchetti A. 
Published: August 2010

SummaryVerapamil, a calcium antagonist, was compared with propranolol, a widely used beta‐adrenoreceptor blocker, in hypertensive patients with respect to its antihypertensive efficacy and incidence and severity of adverse effects.Both drugs caused similar blood pressure reductions without interfering with pulse pressure. The hypotensive effect of verapamil was not accompanied by any effect on heart rate, while after propranolol there was a significant bradycardia. ST‐segment and T wave abnormalities at rest and after exercise were partially or completely reverted by both drugs.The incidence and severity of adverse effects was very low and no patient was withdrawn from the study because of complaints due to the active drugs.Verapamil can be compared as antihypertensive drug to the beta‐blocker propranolol and this may justify, together with the absence of negative effects on lipids, blood sugar, serum electrolytes and renal function, its use as an antihypertensive drug of first choice.
Triglycerides—Main Lipid Risk Factor for Cardiovascular Disease in Women?
Authors: LAPIDUS LEIF , BENGTSSON CALLE , LINDQUIST OLOF , SIGURDSSON JOHANN A. , RYBO ELISABETH 
Published: August 2010

ABSTRACT. Lapidus L, Bengtsson C, Lindquist O, Sigurdsson JA, Rybo E. (Departments of Medicine II and Clinical Chemistry, Sahlgrenska Hospital, Gothenburg University, Gothenburg, Sweden, and Health Centre, HafnarfjÖrdur, Iceland.) Triglycerides—main lipid risk factor for cardiovascular disease in women?A 12‐year longitudinal population study of 1462 women, aged 38–60, was carried out in Gothenburg, Sweden in 1968‐69. Women with high initial serum triglyceride values had a higher 12‐year incidence of myocardial infarction, stroke and total mortality than the others. The findings for serum triglycerides persisted for myocardial infarction, stroke and total mortality after adjustment for other possible risk factors for ischaemic heart disease such as age, systolic blood pressure, smoking, indices of obesity and serum cholesterol, while serum cholesterol did not predict any end‐points studied when taking other risk factors including serum triglycerides into account.
Urinary Excretion of Kallikrein before and after Operation for Aldosterone‐producing Adenoma
Authors: HESSE BIRGER , RASMUSSEN STEN , LUND JENS OTTO , CHRISTENSEN POVL , NIELSEN META DAMKJÆR 
Published: August 2010

ABSTRACT. Hesse B, Rasmussen S, Lund JO, Christensen P, Damkjær Nielsen M. (Department of Clinical Physiology, Glostrup Hospital, and Institute for Experimental Medicine, Copenhagen, Denmark.) Urinary excretion of kallikrein before and after operation for aldosterone‐producing adenoma.Urinary kallikrein excretion (UKal), determined by the esterase method, was measured in 10 normotensive volunteers, 10 patients with essential hypertension and in 7 patients with primary aldosteronism before and after operative removal of the adenoma. UKal values were low in 5 of the patients with essential hypertension. Preoperative UKal values in the patients with aldosteronism did not differ significantly from those of the normal subjects, but decreased in all after operation in parallel with changes in urinary excretion of tetrahydroaldosterone and plasma aldosterone concentration. The study supports the assumption of an association between the renal kallikrein‐kinin system and the mineralo‐corticoid state in man.
Abnormal Renal Sodium Excretion in the Nephrotic Syndrome after Furosemide: Relation to Glomerular Filtration Rate
Authors: DANIELSEN H. , PEDERSEN E. B. , MADSEN M. , JENSEN T. 
Published: August 2010

ABSTRACT. Danielsen H, Pedersen EB, Madsen M, Jensen T. (Department of Internal Medicine C, Aarhus Kommunehospital, and University of Aarhus, Aarhus, Denmark.) Abnormal renal sodium excretion in the nephrotic syndrome after furosemide: relation to glomerular filtratoni rate.The effect of 40 mg furosemide intravenously on sodium excretion, the renin‐aldosterone system and arginine vasopressin (AVP) was studied in 14 patients with the nephrotic syndrome and in 13 control subjects. Creatinine clearance (Ccr) was reduced in all patients but four. Before furosemide, AVP, but not angiotensin II (AII) or aldosterone (Aldo), was increased in the nephrotic patients. After fursoemide, sodium excretion (NaE) increased less and changes in AVP, AII and Aldo were blunted in the patients. Ccr and NaE were positively correlated in the nephrotic syndrome. The reduced sodium response after furosemide in the nephrotic syndrome seems to be closely correlated to a reduced glomerular filtration rate but not to an increased activity of the renin‐angiotensin‐aldosterone system. The reduced response of AVP, AII and Aldo after furosemide is consistent with a lower degree of volume depletion in nephrotic patients.
Alternatives to Optimal Administration of Tablets
Authors: HASSELBALCH H. , JØRGENSEN F. , WAMBERG T. , HEY H. 
Published: August 2010

ABSTRACT. Hasselbalch H, JØrgensen F, Wamberg T, Hey H. (Department of Radiology, Glostrup Hospital, the Dispensary, Royal Veterinary and Agricultural University, Departments of Medicine B and Radiology, Frederiksberg Hospital, Copenhagen, and Department of Clinical Physiology, County Hospital, HillerØd, Denmark.) Alternatives to optimal administration of tablets.This controlled investigation of 27 volunteers compared the effect of cold and lukewarm tap water and carbonated water on the passage through the esophagus of a large circular tablet containing barium sulphate and of the same size and specific gravity as an acetylsali‐cylic acid tablet (Kodimagnylss®). The influence of yoghurt on the passage of the same tablet was also examined. The investigation emphasized the importance of taking tablets together with 100 ml of liquid. A comparison of the transit times for tablets taken together with 100 ml of cold carbonated water and 100 ml of lukewarm tap water showed a significantly better passage when the tablets were taken with cold carbonated water (p=0.01). A similar advantage of carbonated liquids was seen when tablets were taken with 25 ml of lukewarm tap water as compared with 25 ml of cold carbonated water (p=0.01). Administration of a tablet in a tablespoon of yoghurt is a good alternative, even though the bioavailability of certain preparations may be reduced.
The Duration of Oral Anticoagulation after Deep Vein Thrombosis
Authors: SCHULMAN S. , LOCKNER D. , JUHLIN‐DANNFELT A. 
Published: August 2010

ABSTRACT. Schulman S, Lockner D, Juhlin‐Dannfelt A. (Thrombosis Unit, Department of Internal Medicine, and Laboratory of Clinical Physiology, Huddinge University Hospital, Huddinge, Sweden.) The duration of oral anticougulation after deep vein thrombosis.Eighty patients with deep vein thrombosis (DVT) were randomized between our routine duration of oral anticoagulation and 50% reduction thereof, in order to evaluate whether shorter therapy could be given without increased risks. The study was stratified, so that 20 patients with the 1st episode of DVT caused by a temporary risk factor were treated for 1.5 or 3 months, 40 patients with the 1st episode of DVT caused by a permanent risk factor for 3 or 6 months, and 20 patients with the 2nd episode of DVT for 6 or 12 months. When warfarin therapy was discontinued, the patients were followed by means of venous occlusion plethysmography every 3 months for 1 year, and clinically for 15–27 months in the different subgroups. Thromboembolic complications were registered and verified by venography and perfusion lung scan. We could not detect any difference between the groups. The rate of rethrombosis and embolism during 12 and 24 months after cessation of anticoagulant therapy was 8 and 10%, respectively, among the patients with reduced duration of treatment and 8 and 14%, respectively, among those with regular duration. One fatal, warfarin‐induced hemorrhage occurred. It is important to reduce unnecessary extension of oral anticoagulation after DVT in order to minimize the negative side‐effects without increasing the recurrence rate. More extensive trials should be performed to confirm our results and define the optimal duration of treatment.
HYPERTENSION IN PREGNANCY
Authors: Svensson Anders , Andersch Bjöm , Hansson Lennart 
Published: August 2010

ABSTRACT. In the years 1969 — 1973, 0.3% of 17000 unselected non‐diabetic pregnancies were complicated by severe pre‐eclampsia, 0.6% by mild pre‐eclampsia and 0.6% by hypertension in pregnancy. Records from affiliated maternity centers and the hospital were studied for these 261 women and for 260 women with matched normotensive pregnancies.The women with pre‐eclampsia/hypertension in pregnancy had higher blood pressure than the control group very early in pregnancy. The hypertensive women were more often primiparous and they had a slightly higher body weight. The patients with severe pre‐eclampsia were older than the other women (30.4 vs 25.4 years for controls, p < 0.001). Immigrants were not more commonly found in the hypertensive groups, but unmarried mothers were more often seen in the mild preeclampsia and pregnancy hypertension groups, 19.1% and 20.6% respectively compared to 7.7% in the control group (p <0.01). A family history of hypertension was frequently reported in all groups.The most striking characteristic of women with pre‐eclampsia/hypertension in pregnancy was their elevated blood pressure before or very early in pregnancy.
Coronary Atherosclerosis Revisited. A Pathologist's View
Authors: Becker A. 
Published: August 2010

ABSTRACT. For many years the paradigm of coronary atherosclerosis, set by pathologists, was the far‐advanced lesion containing extensive atheromatosis with calcifications. From the point of view of understanding atherogenesis, however, it is much more rewarding to study the coronary artery in patients without clinical evidence of obstructive coronary artery disease. In fact, the normal coronary artery is most revealing in showing discrete intimal changes, which consist of a splitting of the internal elastic lamina accompanied by a proliferation of vascular smooth muscle cells. This process eventually results in the formation of the musculo‐elastic layer. In time the cellular and muscular appearance of this layer gradually transforms into a more densely packed fibrous texture. It is of interest, from a point of view of atherogenesis, that the early atherosclerotic lesions often display the histologic features of the musculo‐elastic layer at the base of the plaque. Hence, these observations support the concept that the basic lesion in coronary atherosclerosis is a proliferation of vascular smooth muscle cells, most likely as a response to injury. To this extent a dysfunction of the endothelial cell barrier may by crucial.The observations also indicate that the mechanisms involved in atherogenesis also may alter vascular tone and hence, may contribute to a »spasmic state» of the coronary arteries. A classification of angina pectoris, on the basis of pathogenesis into organic and spasmic may thus prove to be simplistic.
Coronary Bypass Surgery in Stable Angina Pectoris. A Randomized Study of the Effects on Morbidity, Mortality and Employment
Authors: Frick M.H. , Harjola P‐T. , Valle M. 
Published: August 2010

ABSTRACT. The effects of coronary bypass surgery on morbidity, mortality and employment were assessed in a randomized prospective 5‐year study. Exercise tolerance showed an immediate, striking improvement, which was maintained throughout the follow‐up period. Corresponding patients treated with medical therapy showed no change. More than 40 percent of patients in the surgical group were free from symptoms over the five years. The annual mortality of the surgical patients was 0.8 percent as compared with 4.0 percent in the medical patients (p < 0.05). The annual mortality of the intensively treated medical patients with multivessel disease was not significantly higher than the 3.1 percent for a group of patients with single‐vessel disease followed concomitantly. The rate of work at 5 years after bypass surgery was 47 percent as compared with only 18 percent in the randomized medically treated group (p < 0.01).It is concluded that coronary bypass surgery reduces morbidity and mortality and improves employment.
PATHOPHYSIOLOGIC ASPECTS ‐ HEMODYNAMICS
Authors: Persson Stig 
Published: August 2010

Abstract The hemodynamic situation in congestive heart failure (CHF) is greatly influenced by compensatory mechanisms within the heart itself as well as released from die central nervous system and from the kidneys. These measures are intended to maintain the cardiac output at a level as beneficial as possible and to distribute the blood flow to regions with the largest metabolic demands. Thus the hemodynamic consequences of CHF are reflected in the central circulation as well as in the periphery.Within the heart the Frank‐Starling mechanism, adrenergic stimulation causing increase of heart rate and contractility, and during the chronic course also myocardial hypertrophy are operating. The central nervous and peripheral adaptive measures include increased sympathetic outflow bringing about an increased vasomotor tone with augmentation of pre‐ and afterload, and activation of the renin‐angiotensin‐aldosterone system, where angiotensin II further augments vasoconstriction directly and through central nervous stimulation. This vasoconstriction may be counteracted by humoral factors with vasodilatory properties, such as dopamine, bradykinin, acetylcholine and the metabolic products adenosine and lactic acid. The exact role of these and the possible importance of the antidiuretic hormone, arginine vasopressin, the prostaglandin system and the recently discovered atriopeptin remains to be established.As the compensatory mechanisms may maintain a fairly satisfactory hemodynamic situation at rest, investigations should be performed not only at rest but also during exercise to get an over‐all impression of the cardiac functional state It should be realized, however, that adaptive mechanisms cause the hemodynamics in chronic heart failure to differ from those in the acute phase in many respects. This is true particularly during physical exercise.The great importance of neurohumoral and endocrine factors in the compensatory regulation of the failing circulation warrants the definition of heart failure to be extended to “a failure of the heart to maintain cardiac output at a level which is adequate to meet the metabolic demands of the tissues, with preserved normal filling pressures and with undisturbed neurohumoral and endocrine equilibrium”.
The Effect of the Calcium‐entry Blocker Nifedipine on Cold‐induced Digital Vasospasm
Authors: NILSSON H. , JONASON T. , LEPPERT J. , RINGQVIST I. 
Published: August 2010

ABSTRACT. Nilsson H, Jonason T, Leppert J, Ringqvist I (Department of Internal Medicine, Fagersta Hospital, Fagersta, Department of Clinical Physiology, Västerås Central Hospital, Västerås, Department of General Medicine, Västerås Western Hospital, Västerås and Department of Clinical Physiology, Västerås Central Hospital, Västerås, Sweden). The effect of the calcium‐entry blocker nifedipine on cold‐induced digital vasospasm. A double‐blind crossover study versus placebo. Acta Med Scand 1987; 221:53–60.The effects of the calcium‐entry blocker nifedipine 20 mg, two 10 mg capsules, t.i.d. in patients with cold‐induced digital vasospastic disease of idiopathic or traumatic origin was tested in 28 patients, using double‐blind crossover technique on both symptoms and test results. The effect of treatment on digital blood pressure during local cooling was assessed using the Nielsen‐Lassen method. Symptomatic improvement was reported by 5 patients during placebo treatment and 17 during nifedipine treatment (p<0.01). The symptomatic improvement was significant in the total group of patients and in the group of patients with idiopathic vasospastic disease. The digital blood pressure during local cooling improved significantly with nifedipine at 5, 10, 15 (p<0.001) and 20°C (p<0.05) for the total study population and for the two subgroups except for the change at 20°C in the IDIOP group. At a digital temperature of 10°C, 2 patients reached normal digital blood pressure during placebo treatment compared to 16 during nifedipine treatment (p<0.001). The number of side‐effects increased significantly (p<0.05) during nifedipine treatment. We consider the use of nifedipine in patients with cold‐induced digital vasospastic disease to be of great value, especially in patients with digital vasospastic disease of idiopathic origin.