bluuebunny/crossref_metadata_2025_split huggingface dataset:
Paracetamol (Acetaminophen) Clearance in Patients with Cirrhosis of the Liver
Authors: Andreasen Per Buch , Hutters Lars 
Published: August 2010

ABSTRACT The pharmacokinetics of paracetamol were studied in 11 patients with cirrhosis of the liver and 12 controls. The average biological half‐life after oral administration of 1 g paracetamol was significantly prolonged in patients with hepatic cirrhosis compared to the controls (3.7 hr vs. 2.1 hr) and, correspondingly, the average plasma clearance was significantly reduced from 337 ml × min‐1 in the controls to 162 ml × min‐1 in the patients with cirrhosis of the liver.After subchronic dosing of paracetamol with 1 g paracetamol t. i. d. the plasma half‐lives of paracetamol remained unchanged. Steady‐state levels of paracetamol were significantly increased in the patients with cirrhosis of the liver. A significant correlation between the values of plasma clearance of paracetamol and prothrombin time (r = +0.88), galactose elimination capacity (r = +0.66), plasma albumin (r = +0.47) and plasma clearance of phenazone (r = +0.85) was found. No clinical or biochemical signs of hepatotoxicity were observed during the study.
PHASED ARRAY CARDIAC IMAGING: SYSTEM OPERATION, RESULTS AND CLINICAL ROLE
Authors: KISSLO J.A. 
Published: August 2010

ABSTRACTProper clinical use of real‐time, two‐dimensional echocardiography depends upon three major factors: the clinical questions posed of these imaging devices, the interrelationship of this technique with other imaging techniques and the quality of the ultrasonic image. The Duke experience with this technique has been primarily based on results obtained with a focused, phased array imaging system over the last three years. During this period of time we have observed that high‐resolution, cross‐sectional ultrasonic images of cardiac structures provide unique diagnostic information that is not possible by any other method. Similarly, this type of information allows the clinician to pose new questions concerning the use of diagnostic ultrasound in patient care. Improvements in image quality that have accompanied the addition of new scan formats and a broad‐band transducer have enhanced the clinical reliability of diagnostic information.
CROSS‐SECTIONAL ECHOCARDIOGRAPHIC EVALUATION OF CHANGES IN VENTRICULAR SHAPE IN THE ISCHAEMIC AND NON ISCHAEMIC LEFT VENTRICLE
Authors: WEYMAN A. E. 
Published: August 2010

SUMMARYM‐mode echocardiography is a useful method for estimating left ventricular volumes and determining multiple parameters of left ventricular function in the symmetrically contracting, normally shaped ventricle. In many clinical situations, however, the shape of the ventricle may be altered or distorted in such a way that the basic M‐mode diameter or dimension of the ventricle is no longer reflective of overall left ventricular volume or function.Cross‐sectional echocardiography is a valuable method for detecting abnormalities in left ventricular shape and thereby defining those cases in which the M‐mode method may not accurately reflect ventricular size or performance. In this report two examples of abnormalities in ventricular shape are described. These include the marked alteration in left ventricular conformation which occurs when aneurysm formation complicates ischemic heart disease and the more subtle changes in ventricular shape seen in patients with both absolute and relative right ventricular volume overload, due to alteration in septal position. These examples illustrate the value of cross‐sectional echocardiography in defining abnormalities of left ventricular shape, indicating situations in which the M‐mode ehocardiographic determinations of ventricular volume and function may be misleading and explaining changes in the patterns of wall motion observed by M‐mode echocardiography which are due to alterations in the shape of the left ventricle.
The Diagnosis of Atrial Myxomas
Authors: Schlossman D. , Selin K. , Wallin J. , Wallentin I. 
Published: August 2010

ABSTRACT. Altogether seven patients with the preoperative diagnosis of atrial myxoma were admitted to our hospital in 1968–78 and referred for surgery. In two patients no tumour was found at operation. In one of them the reason for the misinterpretation was severely malformed mitral leaflets. In the other the contrast medium was injected into a pulmonary vein, which caused a contrast defect due to inadequate mixing.Acta Med Scand 208: 349, 1980.
NONINVASIVE DIAGNOSIS AND ASSESSMENT OF VENTRICULAR SEPTAL DEFECT BY DOPPLER ULTRASOUND
Authors: Hatle L. , Rokseth R. 
Published: August 2010

ABSTRACTThe presence of ventricular septal defect can be diagnosed noninvasively by Doppler ultrasound. Care must be taken to distinguish between VSD and infundibular pulmonary stenosis. VSD was easily differentiated from other cardiac lesions. In 55% of the patients a pressure drop across the VSD, comparable to that present, could be calculated from maximal velocity recorded. In the remaining patients velocity and pressure drop were underestimated, probably due to a too large angle between ultrasound beam and velocity. Pulmonary artery systolic pressure was correctly estimated from Pc‐To interval and heart rate, and RPEP/RVET indicated whether normal or raised diastolic pressure was present in most patients.
CAN ACETYLSALICYLIC ACID ALONE PREVENT ARTERIAL THROMBOEMBOLISM? A PILOT STUDY IN PATIENTS wITH AORTIC BALL VALVE PROSTHESES
Authors: Dale Jon , Myhre Erik 
Published: August 2010

ABSTRACTEncouraged by the effective prevention of arterial thromboembolism with a combination of ASA and anticoagulants (9), the present study was done in 77 patients with a single Starr‐Edwards aortic ball valve. They received one gm. of ASA daily, then the dose of anticoagulants was reduced gradually and the drug discontinued on average five weeks later. Six arterial embolic episodes occurred in five patients, the incidence being 14.5 complications per 100 patients per year. Five emboli were cerebral, none of them serious, and one was removed from a femoral artery. Four of the embolic episodes occurred in three of the 11 patients with continuous arrhythmia, probably from venous thrombi that developed in the left atrium. The occurence of only two embolic complications in the 66 patients with sinus rhythm suggests some prevention of arterial thrombus formation on the prosthetic valves. The results indicate that ASA is inferior to anticoagulants in patients with arrhythmia, while it may represent an alternative to anticoagulation in individuals with sinus rhythm. we prefer, however, the combined thereapy in patients with aortic valve prostheses because of the strong anti‐thrombotic effect achieved by this treatment.
CORONARY HEART DISEASE IN NORWEGIAN SEA‐PILOTS; PART OF THE OCCUPATIONAL HAZARD?
Authors: Erikssen Jan , Johansen Arne Høiem , Rodahl Kaare 
Published: August 2010

ABSTRACTA near maximal bicycle exercise test revealed a prevalence of positive exercise ECG's of 8/68 among apparently healthy sea‐pilots and 93/2014 among apparently healthy men of comparable age in Oslo (P<0.01). This difference could not be explained in terms of differences in commonly accepted coronary heart disease risk factors (cholesterol/triglycerides, smoking habits and blood pressure).Reasons for the difference should be sought in the working environment of the pilots as well as in possible unfavourable life habits adapted during leisure time as indicated by a relative increase in body weight and somewhat lower working capacity in pilots than in age matched counterparts from Oslo.
URINARY FINDINGS AND RENAL FUNCTION IN HYPERTENSIVE AND NORMOTENSIVE WOMEN
Authors: Sigurdsson Johann A. , Bengtsson Calle 
Published: August 2010

ABSTRACT As found from a population study of women, those with arterial hypertension reported more often a history of toxaemia in pregnancy and had more often proteinuria, bacteriuria and impaired renal concentrating capacity than normotensive women. Serum potassium was found to be lower in treated as well as in untreated hypertensive women than in normotensive women.There are many experimental data suggesting that the kidneys play a fundamental role in the pathogenesis of essential hypertension. However, less is known about the role of the kidneys from clinical and epidemiological points of view. This is especially true for women. The aim of this study is to compare renal function and findings from some urinary tests in hypertensive women with those in a normotensive reference group, using epidemiological methods.
The Heart Cell—Electrophysiological Aspects
Authors: Andersson K‐E 
Published: August 2010

AbstractA short review is given of the ionic fluxes associated with the action potential in Purkinje fibres, and in sinus and AV‐node, and of the influence of variations in the extracellular concentrations of K+, Na+, Ca2+and Mg2+on basic electrophysiological parameters.Variations in serum potassium concentration often play an important role in the genesis of arrhythmias by changing several electrophysiological parameters, whereas only extreme variations in the serum calcium level produce electrophysiological effects of clinical importance. Hypo‐ and hypernatremia within the ranges observed clinically most probably do not produce significant electrophysiological changes. Variations in extracellular magnesium concentration seem to have effects on electrophysiological parameters particularly when they occur simultaneously with changes in the concentrations of calcium and potassium.
Systemic Alkalosis and Digitalis Related Arrhythmias
Authors: Brater D. Craig , Morrelli Howard F. 
Published: August 2010

AbstractReviews of large series of patients with digitalis‐induced arrhythmias create a seeming paradox: Hypokalemia is infrequently associated with digitalis‐induced arrhythmias but the clinical benefit of supplementation of potassium for most digitalis‐induced arrhythmias is obvious. Examination of the electrophysiologic abnormalities induced by digitalis coupled with the electrophysiologic effects dependent on the ratio of intracellular to extracellular concentrations of potassium clarifies the issue. We present evidence that supports additive effects of the toxicity of digitalis and abnormal ratios of concentrations of potassium inside and outside the cardiac cell using metabolic alkalosis as a marker of intracellular potassium depletion. Patients with metabolic alkalosis and normokalemia with “therapeutic” concentrations of digoxin had significantly greater prevalance of arrhythmias than did patients without alkalosis. We presume this effect of alkalosis to be mediated by effects on extra‐to intracellular ratios of potassium.
Malignant Arrhythmias in Relation to Serum Potassium Values in Patients with an Acute Myocardial Infarction
Authors: Nordrehaug Jan Erik 
Published: August 2010

AbstractThe results presented here confirm that patients with A.M.I. who are also hypokalemic have an increased risk of cardiac arrhythmias, in particular, V.F. It is also suggested that for patients with low potassium values the risk is due to the hypokalemia and not the diuretics.
Diuretic Treatment and Magnesium Losses
Authors: Wester Per Ola , Dyckner Thomas 
Published: August 2010

AbstractTherapy with most kinds of diuretics causes increased urinary excretion of both potassium and magnesium and after long term treatment the skeletal muscle content of these ions is reduced. Magnesium is known activator of Na‐K‐ATP:ase, which provides the energy for the sodium‐potassium pump. Thus, lack of magnesium may impair the pumping of sodium out from the cell and potassium into the cell. Three studies are presented which agree with this theory. In one study the correlation between potassium in serum and potassium in muscle was, among other factors, found to be dependent on the content of muscle magnesium. In another study it was found in hypokalemic patients that muscle potassium could not be corrected by potassium supplementation if there was a concomitant magnesium deficiency. In the third study it was found that muscle potassium increased after magnesium infusion but not after potassium infusion.
ENERGY METABOLISM IN THE REVERSIBLE AND IRREVERSIBLE PHASES OF SEVERE MYOCARDIAL ISCHEMIA
Authors: Reimer Keith A. , Jennings Robert B. 
Published: August 2010

ABSTRACTHigh energy phosphate (HEP) utilization and depletion as well as the production and distribution of catabolic products of adenine nucleotides were studied in ischemic dog hearts in order to characterize the transition from reversible to irreversible cell injury. Severe ischemia, induced by coronary occlusion in vivo was compared to total ischemia, in vitro. Much of the creatine phosphate (CP) was lost within the first one to three minutes. During severe ischemia in vivo, adenosine triphosphate (ATP) was depleted to only 35% of control by 15 minutes (when myocytes are still reversibly injured) and to less than 10% by 40 minutes (at which time irreversible injury has occurred). HEP production from anaerobic glycolysis was estimated from the rate of accumulation of myocardial lactate. HEP production ceased when the ATP was less than 0.4 μmol/g wet weight (control = 5–6). Prior to this time, 80% of the HEP which had been utilized in ischemia had been derived from anaerobic glycolysis whereas 20% came from pre‐existing stores of CP and ATP.ATP depletion was paralleled by dephosphorylation of adenine nucleotides. The lost nucleotides were recovered stoichiometrically as adenosine, inosine, hypoxanthine, and xanthine in both models of ischemia. When myocardium was reperfused after 15 minutes of ischemia, these nucleosides and bases were lost to the systemic circulation, and repletion of adenine nucleotides was incomplete for as long as four days, apparently because both de novo and salvage pathways of adenine nucleotide synthesis are slow in myocardium.Further studies were done to assess the nature of the associations between the decreasing ATP of the ischemic tissue and the onset of defects in high energy phosphate regeneration, cell volume and ion regulation, and/or membrane permeability. Slices of control tissue from tissue injured by various periods of total ischemia were incubated in oxygenated Krebs Ringer's phosphate medium containing 14 C‐inulin. As long as the ATP of the tissue was not depleted below 5 μmoles/g dry weight prior to incubation, no cellular abnormalities were detected. However, lower ATP levels were associated with depressed high energy phosphate resynthesis and failure of cell volume regulation. Overt membrane damage, as measured by an increased inulin diffusible space, was detected after the tissue ATP content decreased to less than 2.0 μmoles/g dry weight. Thus, cellular viability (reversible injury) was retained despite a modest and persistent ATP depletion, but there was a close assocation between marked ATP depletion and the failure of the damaged tissue to regenerate high energy phosphates and to preserve cell volume and ionic regulation (irreversible injury).
PROSTAGLANDINS AND PLATELET AGGREGATION
Authors: Smith J. B. 
Published: August 2010

ABSTRACTProstaglandins may induce or inhibit platelet aggregation and constrict or dilate blood vessels. Recent interest has focussed on prostaglandins which are derivatives of arachidonic acid including prostaglandin endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2and prostacyclin. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation whose enhanced production by vessel walls should be beneficial. It now appears that the circulating levels of PGI2in man are extremely low and little is known about the manner in which to increase them. Furthermore, aspirin, in doses of as little as 4 mg/kg inhibits prostacyclin as well as thromboxane formation. Thromboxane A2may be involved in coronary ischemia because it is a potent vasoconstrictor that is biosynthesized during platelet aggregation. Although thromboxane A2is very unstable indirect evidence obtained by using thromboxane A generating systems or a stable analogue called carbocyclic thromboxane A2(CTA2) suggests that it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow.The stable prostaglandins PGD2and PGE2are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2inhibits platelet aggregation.
ACUTE INTERVENTION WITH METOPROLOL IN MYOCARDIAL INFARCTION
Authors: Hjalmarson Å 
Published: August 2010

ABSTRACTStudies in experimental and clinical myocardial infarction support the idea that sympathetic activity and myocardial noradrenaline release play a significant role in the development of myocardial ischemic damage.Betablockade has been shown to limit infarct size and lower the incidence of ventricular fibrillation in experimental models. Betablockade to patients (pts) with acute myocardial infarction (AMI) has been shown to reduce ischemia reflected as reduction of ischemic chest pain, decrease ST‐segment elevation and increase lactate extraction. Whether this treatment in the clinical situation can prevent development of infarction, reduce infarct size and early mortality in man remains to be proven.In Gøteborg a double‐blind study on metoprolol and placebo was started four and a half years ago. Inclusion of pts. in the study has been terminated and survival data will be available by May 1, 1981.1395 pts. were included of whom 800 developed AMI. Metoprolol 15 mg was given IV followed by a total daily dose of 200 mg/day. The tolerance for betablockade was generally good.Analysis of serum enzyme estimations of maximal LD I + II showed a significant reduction by metoprolol when the treatment was given within 12 hours of onset of pain. In a subgroup consisting of 103 pts. with AMI metoprolol had no clearcut effects on the ventricular arrhytmias during the first 24 hours in hospital. The betablockade resulted in a 15% reduction in heart rate.The main objective of this study, the mortality during three months of blind treatment will be published late in 1981.
ACUTE INTERVENTION STUDIES IN PATIENTS WITH MYOCARDIAL INFARCTION USING ATENOLOL, PROPRANOLOL, OXPRENOLOL AND DISOPYRAMIDE PHOSPHATE
Authors: Wilcox R. G. 
Published: August 2010

SUMMARYThe value of beta‐blockade and of disopyramide phosphate in the immediate treatment of patients with suspected acute myocardial infarction was assessed in two placebo controlled trials. In the first study 388 patients with suspected acute myocardial infarction were randomly allocated to treatment with propranolol, atenolol, or placebo, and when analysed on an initial intention to treat basis there was no significant difference between the three groups in respect of the mortality at one year. In addition, there was no evidence to suggest that either atenolol, or propanolol reduced the incidence of ‘serious’ ventricular arrhythmias in the coronary care unit.In the second study 473 patients with suspected acute myocardial infarction were randomly allocated to treatment with oxprenolol, disopyramide phosphate, or placebo. Again no significant differences were seen with respect to the mortality at six weeks. There was, however, a significantly increased incidence of heart failure in the group which received disopyramide phosphate. Patients who received this drug also showed a reduced number of dysrhythmic episodes on 24‐hour ECG recordings, but this trend did not achieve statistical significance.These results suggest that none of the three beta‐blockers tested nor disopyramide phosphate is likely to reduce the mortality from acute myocardial infarction when given prophylactically, although disopyramide phosphate does reduce the incidence of ‘serious’ ventricular arrhythmias.
THE NORWEGIAN MULTICENTER STUDY ON TIMOLOL AFTER MYOCARDIAL INFARCTION ‐ DESIGN, MANAGEMENT AND RESULTS ON MORTALITY
Authors: Pedersen Terje 
Published: August 2010

ABSTRACTA cooperative clinical trial involving 20 hospitals in Norway was carried out to establish the effect of timolol (10 mg twice daily) compared with placebo in patients surviving acute myocardial infarction (AMI). The study was conducted in a randomized double‐blind manner.All patients 20–75 years of age admitted to the centers with suspected AMI were registered and screened for the qualifying diagnosis. If the diagnosis of AMI was confirmed, the patients were evaluated for inclusion into the trial 6–27 days after onset of symptoms when being clinically stable. Of the 3647 patients evaluated, 1763 (48.3 %) had one or more of the criteria for exclusion from entry. These were contraindications to betablockade (18 %), serious disease impeding follow‐up (7 %), need for betablockade (9 %), need for other concomitant treatment not allowed (e.g. anti‐arrhythmics) (4 %) or administrative reasons and unwillingness to participate (10 %). The remaining, 1884 patients (51.7 %) were randomly allocated to treatment with timolol (945) or placebo (939) the morning after the evaluation.Patients were stratified into 3 risk groups. In Risk Group I were patients with more than one infarction, Risk Group II were patients with a first AMI at high risk of late cardiac death and Risk Group III were patients with a first AMI at low risk. Clinical examination was done after 1, 3 and 6 months, thereafter every 6 months. Follow‐up time ranged from 12 to 33 months. The groups were comparable with respect to important baseline characteristics.There were 152 deaths in the placebo group and 98 in the timolol group in the entire series. The life table cumulative probability of total death over 33 months was 21.0 % in the placebo and 13.3 % in the timolol group, corresponding to a reduction of 39.4 % (p=0.0003). The number of patients withdrawn from the trial medication was 219 in the placebo and 275 in the timolol group (p<0.01). The number of deaths during the first 28 days after withdrawal was 19 in the placebo group and 12 in the timolol group. When restricting the analysis to death occurring while the patient was taking the test medication or within 28 days of withdrawal («per protocol») there were 117 deaths in the placebo and 67 in the timolol group. The life table cumulative probability of death analysed per protocol was 17.5 % and 10.6 % in the placebo and timolol groups corresponding to a reduction of 39.3 % (p=0.0005).
Control of Circulation by Cerebral Catecholaminergic and Histaminergic Mechanisms
Authors: Karppanen Heikki 
Published: August 2010

ABSTRACT.Catecholamines are formed, released and metabolized in the cerebral regions known to regulate the cardiovascular system. The release of catecholamines in these brain areas is associated with changes in cardiovascular function. Injections of exogenous catecholamines into certain brain regions induce cardiovascular changes and mimic the effects of the release of endogenous catecholamines in the same regions. In addition, drugs with selective effects on cerebral catecholamine functions also induce cardiovascular changes. Changes in cerebral catecholamines have also been found in arterial hypertension. Taken together, these observations provide strong evidence that cerebral catecholaminergic mechanisms have a crucial role in both the normal and pathological control of circulation. Cerebral catecholaminergic mechanisms also mediate, at least in part, the therapeutic effects of clonidine, alpha–methyldopa and some other antihypertensive drugs.Recent findings suggest that histaminergic mechanisms in the brain may also be important in the control of circulation and in the mediation of drug effects. Since the cerebral mono–aminergic systems are necessary for the physiological control of circulation, it is likely that the cerebral catecholaminergic and possibly histaminergic pathways are also involved in the mediation of the effects of psychosocial stress factors on the cardiovascular system.