bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protein Correction of Serum Calcium in Mild Primary Hyperparathyroidism
Authors: Transbøl Ib , Christiansen Claus , Hornum Ib 
Published: August 2010

ABSTRACT Simultaneous determinations of serum total calcium (TOCa), protein corrected total calcium (TOCac), ultrafiltrable calcium (UFCa) and ionised calcium (Ca++) were undertaken in 63 controls and in 76 patients with primary hyperparathyroidism. Raised levels of Ca++ were used as one criterion of the diagnosis which was confirmed by operation in all.For the purpose of estimating the relative value of TOCa and TOCac in the detection of mild hyperparathyroidism we selected all patients with TOCa values below 3.00 mmol/1 (n = 46). As a group these patients turned out to be mildly hypoproteinaemic (p < 0.01), probably because of high age and complicating conditions. Further subdivision of this group into frank hypcrcalcaemia, borderline hypercalcaemia and normocalcaemia was undertaken according to the respective 99% and 95% confidence limits of normal. Twenty‐seven patients were classified as frankly hypercalcaemic by TOCa as well as by TOCac. The distribution of the remaining 19 patients within the three categories was 1:6:12 as judged from TOCa while TOCac gave a better distinction from normal, 9:4:6 (p < 0.01). This compared well with the classification obtained by UFCa, 10:5:4.It is concluded that TOCac is definitely advantageous to TOCa in the detection of hypercalcaemia in mild primary hyperparathyroidism.
Kidney Function in Acromegaly
Authors: Eskildsen P. C. , Parving H.‐H. , Mogensen C. E. , Christiansen J. Sandahl 
Published: August 2010

ABSTRACT Creatinine clearance and daily urinary albumin and β2‐microglobulin excretion rates (radio‐immunoassays) were measured several times in 14 patients with acromegaly. Eleven patients were treated with bromocriptine, 5 to 55 mg/day. The activity of the disease was assessed by measuring urinary growth hormone excretion (radio‐immunoassay).In agreement with previous investigations we found the creatinine clearance elevated. However, no correlation was found between this variable and the urinary growth hormone excretion. Urinary albumin and β2‐microglobulin excretion rates were not significantly different from our previous results in 27 adults control subjects. There was no correlation between urinary growth hormone excretion and urinary albumin or β2‐microglobulin excretion rates. Bromocriptine treatment reduced urinary growth hormone excretion from 220 to 91 ng/24 hours, p<0.01, but no significant alterations were induced in the above mentioned kidney function variables.
CORRELATION STUDIES BETWEEN EMPLOYABILITY, LEFT VENTRICULAR HEMODYNAMICS AND EXERCISE ECG BEFORE AND AFTER AORTOCORONARY BYPASS SURGERY
Authors: Nitter‐Hauge S. 
Published: August 2010

ABSTRACTThe occupational status of a group of 70 male patients, 30 to 65 years of age, operated with aortocoronary bypass surgery, were studied and related to left ventricular function, number of patent grafts, and exercise ECG using a bicycle ergometer, in connection with a re‐study on an average of 14 months after operation. The patients consisted of two series of males: one series (n = 39) consisted of subjects unable to work (<<non‐active>> group), the other series (n = 31), consisted of subjects actually working up to the time of examination (<<active>> group). The <<non‐active>> group had a higher percentage of men in manual occupations (77 vs 48 %), and most of them had been temporarily or permanently disabled before operation (87 vs 55 %) compared with the <<active>> group. There was no correlation between employability. on the one hand and objective means of left ventricular function as left ventricular end‐diastolic pressure before and after angiography and ejection fraction, and number of patent grafts per patient on the other. The <<active>> group had in general increased their tolerance for exercise, and had a higher exercise capacity than the <<non‐active>> group. In the former series, all but 3 patients had a normal exercise tolerance. The increase in exercise tolerant in the <<non‐active>> group was more modest, and only 1/3 of the patients had a normal exercise capacity. Exhaustion and angina pectoris were the two principally different causes of limiting exercise, in this respect there was no difference between the two groups.
COARCTATION OF THE AORTA. FOLLOw‐UP OF 218 PATIENTS OPERATED ON AFTER 13 YEARS OF AGE
Authors: Forfang Kolbjørn , Rostad Hans , Sørland Svein 
Published: August 2010

SUMMARYTwohundred and eighteen patients aged 13 years or more at operation for coarctation of the aorta were selected for a long‐term postoperative follow‐up study. The mean age at operation was 25,3 years, range 13 to 62 years, and the mean follow‐up period was 13 years, range 2 to 28 years.The surgical mortality rate was 1,4%, all 3 patients being in their fourth decade. There were 35 late deaths (16,3%), 26 having cardio‐vascular disease as the causation; 3 patients developed a dissecting aneurysm of the ascending aorta, and 11 died suddenly of unknown cause. Persisting hypertension was found in approximately one third of the patients. A highly significant correlation was demonstrated between the systolic blood pressures before and after surgery. Aortic valve disease occurred in 31 patients (14,2%).Coarctation of the aorta should be operated on in childhood, and a close postoperative long‐term follow‐up in all patients is recommended.
ATRIAL SEPTAL DEFECTS OF SECUNDUM TYPE IN PATIENTS LESS THAN 40 YEARS OF AGE. A FOLLOw‐UP STUDY
Authors: Rostad Hans , Sørland Svein J. 
Published: August 2010

ABSTRACTThe series comprised 479 consecutive patients from all parts of Norway operated on in the period 1955–1976. Only 8% were less than 7 years at surgery. Dominating preoperative symptoms were dyspnea and increased fatique. The follow‐up period ranged from 2 to 21 years, mean 10,28 years. There were 4 early deaths (within 30 days after surgery), and at follow‐up further 5 patients had died. Excluding a man who died in a traffic accident the total mortality is 1,7%. Of the 470 surviving patients 81,7% were improved, 17% were unchanged and 1,3% had deteriorated. In patients with symptoms dyspnea and palpitations were common complaints. Different types of arrhythmia were found in 31 patients. One third were paroxysmal tachy‐arrhythmias, and 9 patients had atrial fibrillation. Only 3 of the 31 patients had some type of preoperative arrhythmia, and 26 were more than 20 years of age at surgery. Seven patients were reoperated because of a residual left to right shunt, 5 of them were initially operated in hypothermia and inflow occlusion. During the follow‐up period 10 patients had late cardiovascular disorders.
CLASSIFICATION OF CARDIOACTIVE DRUGS IN VIVO BY USING PROGRAMMED ELECTRICAL STIMULATION IN COMBINATION wITH MONOPHASIC ACTION POTENTIAL RECORDINGS AT DIFFERENT PACING RATES
Authors: Landmark Knud , Amlie Jan P. , Refsum Helge 
Published: August 2010

ABSTRACTThe effect of antiarrhythmic drugs on myocardial refractoriness may be due to changes either in Vmaxof phase 0 or the phase of repolarization of the AP or both. By using programmed electrical stimulation in combination with MAP recordings at different pacing rates in the intact dog heart, it was possible to classify and to a certain extent to elucidate the mode of action of various cardioactive drugs in vivo.Vaughan williams (68, 69) has proposed that antiarrhythmic drugs possess one or more of four main classes of action. The first class of action (quinidine may be regarded as the prototype) is a direct membrane effect which restricts the fast sodium current (the fast component) and thereby Vmaxof the AP in the absence of significant changes in MDP (30, 32, 67, 73). The second class causes β‐adrenergic receptor blockade, the third class increases the AP duration (amiodarone may be regarded as a prototype (62)) and the fourth class modifies the inward calcium current during the excitation period (6, 20, 21, 33). Classification of antiarrhytmic drugs have been based primarily on their effects on AP duration and amplitude, Vmax, membrane responsiveness (the relationship between MDP and Vmax), conduction and refractoriness in vitro and in vivo (56).The duration of the AP has been regarded as a valuable determination of the refractory period (28, 72) and it has been shown that the ERP of isolated dog Purkinje fibres ends when the repolarization has restored the transmembrane AP to a value of ‐55 to ‐65 mV (28). However, the correlation between the process of repolarization and the reactivation of the sodium carrying system is not always constant, and the effects of certain antiarrhythmic agents have been attributed partly to a change in this relationship (67). Thus, drugs with first class action shift the values relating Vmax(ordinate) to MDP (abcisse) to the right, indicating that fewer sodium carriers are available at all membrane potentials (61, 73).In assessing the mode of action of cardioactive drugs on the myoardium, it is therefore necessary to combine different experimental techniques and procedures. The present work was carried out to study the effects of different drugs on the refractoriness of the right ventricle of the dog heart and to see if any changes were correlated to alterations in the duration of the MAP. For this purpose we used programmed electrical stimulation in combination with MAP recordings at different pacing rates.
PHARMACOLOGICAL EFFECTS ON CORONARY HAEMODYNAMICS: A COMPARATIVE STUDY BETWEEN ATENOLOL, VERAPAMIL, NIFEDIPINE AND CARBOCROMEN
Authors: Simonsen Svein 
Published: August 2010

ABSTRACTEffects on coronary haemodynamics were investigated in patients with ischaemic heart disease. Investigations were performed at rest and during a cardiac stress test provoked by atrial pacing to submaximal heart rates. The effects of 4 drugs used in the treatment of angina pectoris were studied.The continuous infusion thermodilution method was used to measure left ventricular venous drainage.CVF was significantly increased by atrial pacing, both in the GCV and in the CS.Atenolol reduced CVF and MVO2 at rest, but had no effect during atrial pacing. The decrement in flow and oxygen consumption effected by the drug could be attributed solely to a reduction in heart rate and therefore in left ventricular work. No direct effect on CAR could be identified.Both injection (verapamil) and sublingual (nifedipine) application of calcium antagonists gave a weak coronary vasodilatory effect at rest, but not during cardiac stress. No oxygen saving effect could be demonstrated as both MVO2 and MVO2 per unit left ventricular work was totally unaffected by the drugs. Neither was there any effect on the major general haemody‐namic determinants of oxygen demand.Carbocromen was found to be a potent coronary vasodilator both at rest and during atrial pacing. This did not result in any change in MVO2 as there was a parallel decrease in coronary arteriovenous oxygen difference. Investigations performed during angina pectoris demonstrated metabolic evidence of increased ischaemia after carbocromen which may be due to to a <<coronary steal>> effect.The present study demonstrated that interventions may influence left ventricular oxygen consumtion in a favourable way. On the other hand no effects, or even untoward effects, are exerted by substances which are in use today in patients with coronary heart disease.
Circulatory Effects of Stress in Essential Hypertension
Authors: Andrén Lennart , Hansson Lennart , Section Hypertension 
Published: August 2010

Abstract: Hemodynamics and plasma catecholamines were studied during mental arithmetics and cold pressor test in thirteen patients with essential hypertension. Blood pressure was significantly increased by both forms of “stress”. Cold pressor test caused a significant increase in total peripheral resistance, while mental arithmetics increased heart rate and cardiac output significantly. Thus, different forms of “stress” can increase blood pressure by totally different hemodynamic mechanisms.Acute cardioselective and non‐selective beta‐receptor blockade did not affect the hemodynamic reaction pattern during cold pressor test. The increase in heart rate and cardiac output during mental arithmetics was blocked by non‐selective but not with cardioselective beta‐blockade. Both beta‐blockers were, however, inefficient in preventing the blood pressure elevation induced by mental arithmetics. Plasma noradrenalin was significantly increased during mental arithmetics after both cardioselective and non‐selective beta‐blockade compared to placebo. During cold pressor test there was a significant increase in noradrenalin only after non‐selective beta‐blockade. Adrenalin in plasma was significantly incre sed only during mental arithmetics after cardioselective beta‐blockade.The pathogenesis of essential hypertension is complex and still not fully understood. Both hereditary (1) and environmental factors such as salt intake (2) and stress (3,4,5) are probably of importance as risk factors for essential hypertension.Animal studies have shown that different forms of stress can produce permanent hypertension due to structural changes in the resistance vessels (6). Against this background we decided to investigate acute hemodynamic effects of two well‐defined types of “stress”, e.g. mental arithmetics and cold pressor test in patients with essential hypertension and to study if the hemodynamic reactions could be modified by cardioselective and non‐selective beta‐receptor blockade. Catecholamines in plasma were studied before, during and after “stress”.
PRESSURE NATRIURESIS IN HYPERTENSION.
Authors: Omvik Per 
Published: August 2010

ABSTRACTPressure natriuresis, defined as the relationship between sodium excretion and mean arterial pressure (MAP), was assessed during graded reduction of arterial pressure with nitroprusside in 16 essential hypertensives (EH). In all patients, sodium excretion fell linearly with reductions in arterial pressure (r > 0.68; p < 0.05). The per cent change of sodium excretion from control per mmHg change in MAP (δUNa V/δMAP) was less in patients with resting MAP above 120 mmHg than in those with lower blood pressure (1.4 ± 0.1 versus 3.0 ± 0.3; p < 0.001), but the pressure at which urine flow extrapolated to zero (75 ± 3 mmHg) was not significantly different in the two groups.The slope of the relationship between sodium excretion and arterial pressure was significantly correlated with resting MAP (r = −0.67; p < 0.05) and with plasma volume (r = 0.61; p < 0.05). Furthermore, the ratio δUNa V/ δMAP also rose in concert with body fluid volumes when a salt load of 8 g of sodium chloride was added to the regular diet. Thus, the sensitivity of pressure natriuresis was determined by level of resting arterial pressure and body fluid volumes. These experiments suggest that two mechanisms might be activated in EH to avoid dangerous sodium and volume depletion: 1) attenuation of pressure natriuresis at higher levels of arterial pressure, and 2) blunting of pressure natriuresis by volume contraction. By this hypothesis, the lower slope of pressure natriuresis is secondary to hypertension rather than its cause.
Potassium Supplementation in the Treatment of Ventricular Arrhythmias
Authors: Rowland Edward , Krikler Dennis M. 
Published: August 2010

AbstractPotassium has a fundamental role in the regulation of the action potential in both myocardial and specialized cardiac cells. The frequency and diversity of ventricular arrhythmia associated with hypokalemia suggests that potassium also plays a crucial part in the genesis of many cardiac arrhythmias. In addition, the presence of potassium in adequate amounts is required for the effective action of many antiarrhythmic agents.While more information on the mechanism of ventricular arrhythmias in the human is required, as well as observing local biochemical status in the myocardium, it would appear that maintaining the serum potassium towards the upper limit of the normal range offers a logical adjunct to the drug treatment of ventricular arrhythmias.
Relation between Potassium, Magnesium and Cardiac Arrhythmias
Authors: Dyckner Thomas , Wester Per Ola 
Published: August 2010

AbstractMagnesium may influence the incidence of cardiac arrhythmias by

a direct effect
an effect on potassium metabolism
an effect as a calcium blocking agent.

In the event of a magnesium deficiency the cell cannot attract potassium against the transmembrane concentration gradient. The reason may be that a magnesium deficiency interferes with the function of membrane ATPase, and thus the pumping of sodium out from the cell and potassium into the cell is impaired. The interference from a magnesium deficiency on the equilibrium of potassium between the intra‐ and extracellular spaces may result in changes in the resting membrane potential, changes in potassium conductance across the cell membrane as well as disturbances in the repolarization phase.
SIGNIFICANCE OF PLATELET FUNCTION AND THROMBOXANE B2 LEVELS ACROSS THE HUMAN MYOCARDIAL VASCULAR BED
Authors: Mehta Jawahar , Mehta Paulette 
Published: August 2010

ABSTRACTThere is an intense interest in the role of platelets in the pathogenesis of myocardial ischemia. To determine platelet function in coronary circulation and the influence of various platelet‐active drugs, we have studied large number of patients with coronary disease (CD) defined as >50 % luminal narrowing and subjects with normal coronary arteries (NCA). Blood samples were collected from aorta (Ao) and coronary sinus (CS) at rest, during and following atrial‐pacing induced tachycardia characterized by ECG changes and symptoms. Platelet aggregation (PAg) using epinephrine (E) and adenosine diphosphate (ADP) as stimulating agents and platelet counts were performed. In CD patients CS blood had lower (Pd<0.01) PAg (E‐59 ± 8, ADP‐49 ± 7 %) than Ao blood (E‐74 ± 6, ADP‐68 ± 7 %). Platelet counts in CS blood (173,000 ± 16,000/mm3) were lower (P<0.01) than in Ao blood (233,000 + 30,000/mm3). In NCA patients, the CS and Ao platelet counts and PAg were not significantly different. During tachycardia stress PAg and counts were unaltered in NCA patients. In contrast in CD patients PAg increased significantly (P<0.05) in CS but not in Ao blood during stress and returned to baseline following tachycardia implying platelet activation during stress‐induced myocardial ischemia. Oral aspirin 650 mg abolished the differences in Ao and CS blood PAg (CS‐E 51 ± 8, ADP 54 ± 7%; Ao‐E 45 ± 8, ADP 55 ± 8 %), and in counts (CS‐221,000 ± 8,000/mm3; Ao‐230,000 ± 71,000/mm3) in CD patients. Aspirin also significantly decreased tachycardia‐related increase in PAg in CS blood. Administration of intravenous dipyridamole 25 mg in 8 other CD patients, resulted in increase in platelet counts in CS from 255,000 ± 29,000 to 286 ± 34,000/mm3 and in PAg from 30 ± 8 to 52 ± 9 %, while Ao blood counts and PAg were unchanged, so that the differences in Ao and CS platelet counts and aggregation were abolished. In other studies, we compared CD patients treated with and without propranolol. Propranolol‐treated patients had lower PAg in Ao as well as CS blood compared to non‐treated patients, but the gradients in PAg and counts between Ao and CS blood was still present. However, tachycardia‐related increase in CS PAg was markedly less in CS blood in propranolol‐treated patients compared to non‐treated patients.These data show that 1) gradient in platelet counts from Ao to CS exists related probably to platelet aggregate formation in atherosclerotic vessels, 2) activation of platelets leads to low PAg activity in CS blood, 3) tachycardia stress is associated with platelet activation at the level of myocardial vascular bed, 4) aspirin and dipyridamole modify these gradients, 5) aspirin blunts tachycardia‐related increase in CS PAg, 6) propranolol has potent PAg inhibitory effects and modifies platelet response to tachycardia stress.
BETA BLOCKERS IN EXPERIMENTAL MYOCARDIAL INFARCTION
Authors: Nayler Winifred G. 
Published: August 2010

ABSTRACTWidespread interest has developed in the possibility of using beta‐adrenoceptor antagonists to protect the myocardium against the deleterious consequences of an impaired coronary blood flow. The consequences include loss of active tension generating capacity, impaired mitochondrial function, destruction of tissue ultrastructure and loss of ionic homeostasis. The ionic imbalance includes loss of tissue K* and gain in Na* and Ca2+.Under conditions of low flow, or when coronary flow is absent, a loss of K* from the cell must result in a localized increase in extracellular K*. This, in turn, may be sufficient to trigger arrhythmias. Theoretically beta‐adrenoceptor antagonists should protect against such an ischaemic induced increase in extracellular K*. To test this hypothesis isolated Sprague‐Dawley rat hearts have been pretreated with either timolol (25 μg/ 1) or propranolol (100 μg/1). The hearts have then been made ischaemic at 37°C for 60 minutes and then reperfused. Coronary effluent collected during the first 5 minutes reperfusion showed a significant (p<0.001) increase in K*. This increase in coronary K* was attenuated by prior β‐blockade. Adding the beta blockers during the phase of reperfusion had no effect on the rate of K* loss. The significance of these results will be discussed with reference to the use of beta‐adrenoceptor antagonists for the protection of ischaemic heart muscle.
EARLY ANGIOGRAPHY DURING INFARCTION: A SEARCH FOR SPASM
Authors: Gold Herman K. , Leinbach Robert C. 
Published: August 2010

ABSTRACTThe predominant cause of continuing injury during transmural myocardial infarction is intracoronary thrombosis linked to plaque rupture or plaque hemorrhage. The initiating events, however, remain unknown primarily because angiography is performed late. Postmortem analysis of patients dying suddenly may not be relevant since it is not known whether a transmural myocardial infarction would have followed. Therefore, we must make conclusions from early therapeutic responses and from angiography performed always with some delay.Sixty patients were studied. Twenty‐five showed anterior transmural infarction and were evaluated by systemic nitroglycerin response, followed by coronary angiography after six hours to seven days. Only three of twenty‐five showed greater than 50 % reduction in precordial ST segment elevation during the thirty‐minute postnitroglycerin observation period. Angiography showed left anterior descending occlusion in thirteen and high grade stenosis in twelve. Nitroglycerin response was seen only in patients with left anterior descending stenosis. The mechanism of nitroglycerin response, however, was not observed.Thirty‐five patients with either anterior or inferior transmural infarction received sublingual and intravenous nitroglycerin on admission and coronary angiography within six hours, during which intracoronary nitroglycerin was infused into the obstructed coronary artery. Only two patients responded to systemic nitroglycerin with a greater than 50 % fall in ST segment elevation. At angiography the offending vessel was stenotic and not further dilatable with intracoronary nitroglycerin. Thirty‐two patients receiving intracoronary nitroglycerin showed no reduction in coronary stenosis and no reversal of obstruction. Three patients with coronary occlusion (two with inferior infarction, one with anterior infarction) responded to intracoronary nitroglycerin with slow antegrade flow. This restored flow was adequate to outline intracoronary filling defects but inadequate to reduce injury or to induce ventricular irritability. In these patients streptokinase infusions cleared the defects and augmented antegrade flow.In conclusion, neither responsivity to nitroglycerin nor early coronary angiography demonstrate that coronary spasm is pronounced after onset of transmural myocardial infarction.