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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Macromolecules 25 (1992), S. 4325-4328 
    ISSN: 1520-5835
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 100 (1978), S. 3190-3197 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 42 (1970), S. 266-267 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 36 (1964), S. 577-579 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 24 (1952), S. 1892-1894 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Macromolecules 28 (1995), S. 3175-3181 
    ISSN: 1520-5835
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Keywords: Mitral and aortic regurgitation ; left ventriculography ; left ventricular volumes ; regurgitant volume ; ejection fraction ; contractility reserve ; Mitral- und Aortenklappenregurgitation ; Ventrikulographie ; linksventrikuläre Volumina ; Regurgitationsvolumen ; Auswurffraktion ; Kontraktilitätsreserve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 2 Patientenkollektiven mit Mitralklappeninsuffizienz (MI,n=20) und Aortenklappeninsuffizienz (AI,n=22) wurden im Rahmen diagnostischer Herzkatheterisierungen intrakardiale Drucke und linksventrikuläre Volumengrößen untersucht (enddiastolisches Volumen, endsystolisches Volumen, Schlagvolumen, Auswurffraktion, Regurgitationsvolumen). Die Befunde wurden mit einem Normalkollektiv (N,n=20) verglichen. 1. Das enddiastolische Volumen war gegenüber der Norm im Mittel um 32% (MI) bzw. 113% (AI) erhöht, das endsystolische Volumen zeigte Zunahmen um 85% (MI) bzw. 181% (AI). Das ventrikulographisch ermittelte totale Schlagvolumen war um 11% (MI) bzw. 86% (AI) gesteigert. Das Regurgitationsvolumen betrug bei AI im Mittel 64% des totalen Schlagvolumens, bei MI 47%. Die Auswurffraktion war in beiden Kollektiven gegenüber der Norm im Mittel um 12–14% erniedrigt. 2. Das enddiastolische Volumen im linken Ventrikel zeigte in beiden Kollektiven (MI, AI) eine deutliche Abhängigkeit von der Höhe des Regurgitationsvolumens. Gleichermaßen nahm das totale Schlagvolumen mit steigendem enddiastolischen Volumen zu. Die Zunahme war bei AI (bis auf 250% der Norm) wesentlich ausgeprägter als bei MI und ist auf eine hämodynamisch wirksame Einbeziehung des Frank-Starling-Straub-Mechanismus infolge vermehrter diastolischer Vordehnung durch das Regurgitationsvolumen hervorgerufen. Eine Korrelation zwischen dem enddiastolischen Volumen bzw. dem Regurgitationsvolumen und dem effektiven Schlagvolumen sowie weiteren Größen der “Vorwärts“-Pumpfunktion (Herzminutenvolumen, Herzindex, Herzarbeit) bestand nicht. Die linksventrikuläre Dehnbarkeit war in den 3 untersuchten Kollektiven (N, MI, AI) annähernd gleich. 3. Die Auswurffraktion des linken Ventrikels blieb mit zunehmendem enddiastolischen Volumen (AI) über einen Bereich bis zu enddiastolischen Volumina von ca. 400 ml weitgehend unverändert und nahm erst bei enddiastolischen Volumina 〉400 ml ab. Bei dekompensierter AI war die Auswurffraktion des linken Ventrikels bereits bei niedrigeren enddiastolischen Volumina herabgesetzt. Dahingegen nahm die Auswurffraktion bei MI im gesamten Bereich enddiastolischer Volumina mit steigendem enddiastolischen Volumen und Regurgitationsvolumen konsekutiv ab. Die erhöhten totalen Schlagvolumina in beiden Kollektiven (MI, AI) sind somit über eine Erhöhung des enddiastolischen Volumens und weniger durch eine vergrößerte Auswurffraktion bedingt. 4. Die im Vergleich zu MI hohe und langdauernde Kontraktilitätsreserve des linken Ventrikels bei kompensierter AI wird u.a. auf die unterschiedliche Kontraktionsform (Verringerung der isovolumetrischen Anspannungsphase und Übergang zur isotonischen Kontraktion mit zunehmender Regurgitation), die erhöhte diastolische Vordehnung (preload) und die Verringerung der mittleren Wandspannung des linken Ventrikels zurückgeführt. Die Kontraktilitätsreserve wird wesentlich von der Inotropie des Myokards bestimmt. Bei Inotropieabnahme sind bei gleicher Kontraktionsform und Ventrikeldimension konsekutive Abnahmen der totalen und effektiven Pumpfunktion des linken Ventrikels nachweisbar.
    Notes: Summary In 2 groups of patients with mitral valvular incompetence (MI,n=20) and aortic valvular incompetence (AI,n=22) intracardiac pressures as well as left ventricular volumes (enddiastolic volume, endsystolic volume, stroke volume, ejection fraction, regurgitant volume) were determined during routine left heart catheterization and left ventriculography. Data obtained were compared with a normal group (N,n=20). 1. Enddiastolic volume was increased by 32 per cent (MI) and 180 per cent (AI) respectively in comparison to normal. Endsystolic volume was increased by 85 per cent (MI) and 113 per cent (AI). Total stroke volume exhibited increases by 11 per cent (MI) and 86 per cent (AI) respectively. Regurgitant volume averaged 64 per cent (AI) of total stroke volume, and 47 per cent in MI. Left ventricular ejection fraction was reduced in both groups by about 12–14 per cent. 2. Enddiastolic volume was significantly dependent on the amount of regurgitant volume in both groups (MI, AI). Likewise total stroke volume increased with increments in enddiastolic volume. This increase was far more pronounced (up to 250 per cent of normal) in AI in comparison to MI and may be referred to an effective contribution of the Frank-Starling-Straubmechanism, induced by increased preload following regurgitation. There existed no correlation between enddiastolic volume or regurgitant volume and the effective forward stroke volume and other parameters of forward pump function (effective cardiac output, cardiacindex, external cardiac work). Left ventricular compliance, as determined by diastolic pressure-volume relationships, was nearly the same in the 3 groups (N, MI, AI). 3. Left ventricular ejection fraction was nearly unchanged with increments in enddiastolic volume over a range of enddiastolic volumes up to 400 ml. At higher enddiastolic volume (〉400 ml) decreases were found. In the failing heart with AI left ventricular ejection fraction was reduced even at low enddiastolic volume, exerted by decreases of fibre shortening and contractility. In contrast, in MI ejection fraction decreased with increments of enddiastolic volume over the whole range investigated. The increase in total stroke volume in both groups therefore was produced by increases of enddiastolic volume and to a very small extent by an increase of the ejection fraction. 4. The large contractility reserve in compensated AI may be referred to the altered contraction mechanism in aortic valvular regurgitation associated with i) decreases of isovolumic pressure development and increase of isotonic contraction, ii) increase of diastolic fibre stretch (preload) and iii) decrease of mean wall tension. Contractility reserve was essentially influenced by myocardial contractility. With decreases of contractility consecutively decreases of the total and the effective pump function of the left ventricle may occur despite unchanged contraction form and left ventricular dimensions.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 311-319 
    ISSN: 1432-1440
    Keywords: Bartter's syndrome ; Tubular function ; Hypokalemia ; Prostaglandins ; Renin-angiotensin-aldosterone system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies have demonstrated that patients with Bartter's syndrome regularly exhibit a reduced tubular absorption of chloride in the ascending limb of Henle. This defect represents the most ‘proximate’ abnormality of the syndrome so far identified. It causes renal potassium loss through reduced potassium cotransport in the ascending limb of Henle as well as through increased tubular flow rate stimulating potassium secretion in the distal nephron. Hypokalemia per se may stimulate renal and vascular prostaglandin synthesis. Prostaglandins in turn mediate the increased activity of the renin-angiotensin-aldosterone system and may also participate in the vascular resistance to the pressor action of exogenous angiotensin II and norepinephrine. The differential diagnosis of Bartter's syndrome includes syndromes with hypokalemic alkalosis and a stimulated renin-angiotensin-aldosterone system such as extrarenal electrolyte losses and diuretic abuse. Extrarenal electrolyte loss can be identified through metabolic studies with determination of urinary electrolyte excretion and by the determination of the fractional free-water clearance during sustained water diuresis. Covert diuretic abuse may be identified through a screen of the urine for the presence of diuretics and by marked day-to-day variations in urinary electrolyte excretion during metabolic studies. The therapcutic approach to Bartter's syndrome includes administration of potassium chloride and potassium-sparing diuretics as well as of inhibitors of prostaglandin synthesis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1440
    Keywords: Na-K-ATPase ; Ouabain ; Natriuretic hormone ; Intracellular electrolytes ; Peripheral vascular resistance ; Cardiac function ; Hypertension ; Calcium entry blockade ; Human studies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An endogenous humoral factor which inhibits the sodium- and potassium-activated adenosine triphosphatase (Na-K-ATPase) enzyme in vitro has been incriminated recently of playing a pathogenetic role in experimental and human hypertension. The present study was therefore performed in six healthy volunteers to investigate the hemodynamic consequences of an inhibition of this enzyme by ouabain, a potent and specific inhibitor of Na-K-ATPase. In addition, the role of intracellular calcium as a potential mediator was studied indirectly by the administration of nifedipine, a potent calcium entry blocker with predominant vasodilator properties. Intravenous administration of 8.5 µg ouabain/kg body weight inhibited red blood cell (RBC) — Na-K-ATPase by 49% which was accompanied by a significant increase in RBC — ATP and a decrease in intracellular potassium concentrations. This enzyme inhibition resulted in a 24% increase in peripheral vascular resistance. The parallel decrease in cardiac output and heart rate, however, prevented a rise in arterial pressure. This increase in vascular resistance was completely abolished by pretreatment with nifedipine (10 mg orally). In the absence of an effect of nifedipine on Na-K-ATPase, its attenuation of the vasoconstrictor effect of ouabain suggests that the effects of ouabain on the vascular smooth muscle cell are mediated by intracellular calcium. These results demonstrate that inhibition of the Na-K-ATPase enzyme in vivo causes a marked peripheral vaso-constriction. They are also compatible with the concept that an endogenous inhibitor of Na-K-ATPase — in the presence of decreased baroreceptor reflex sensitivity due to blood volume expansion — may play a role in the pathogenesis of human arterial hypertension.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 934-943 
    ISSN: 1432-1440
    Keywords: Obstructive nephropathy ; Relief ; Polyuria ; Renal haemodynamics ; Tubular function ; Renin-Angiotensin system ; Prostaglandin-Thromboxane system ; Natriuretic factors ; Harnstauungsniere ; Entlastung ; Polyurie ; Renale Hämodynamik ; Tubulusfunktion ; Renin-Angiotensin-System ; Prostaglandin-Thromboxan-System ; Natriuretische Faktoren
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Eine postobstruktive Polyurie wird nach Entlastung der beidseitigen Harnstauungsniere beobachtet. Nach anfänglicher passagerer Zunahme der Nierendurchblutung bei akuter Obstruktion stellt sich bei chronischer Obstruktion neben der strukturellen und funktionellen Tubulusschädigung eine zunehmende Vasokonstriktion mit erheblich eingeschränkter Nierendurchblutung vor allem des Nierenmarks ein. Sie ist mit einer Aktivierung des Renin-Angiotensin Systems und der renalen Prostaglandin (PG)-Synthese, insbesondere des vasokonstriktorischen Thromboxan A2, vergesellschaftet. Die Störung der exkretorischen Nierenfunktion führt zu Azotämie und Expansion des Extrazellularvolumens (EZV). Zu den Mechanismen, die trotz weiterhin stark eingeschränkter Nierenrindenperfusion und glomerulärer Filtration nach Entlastung der gestauten Niere zur Polyurie führen, gehören die erhöhte Nierenmarkdurchblutung bei gesteigerter medullärer PGE-Synthese, strukturelle und funktionelle Tubulusschädigung mit Hemmung der tubulären Natrium-Resorption und (Vasopressin-resistenter) Störung des renalen Konzentrationsvermögens, osmotische Diurese, Aktivierung natriuretischer Faktoren durch die Expansion des EZV sowie schließlich die iatrogene Überwässerung. Die daraus resultierenden Elektrolyt- und Wasserverluste stellen eine potentielle Gefahr bei der Korrektur der angeborenen oder erworbenen beidseitigen Harnabflußstörung dar und verlangen eine exakte Überwachung der Patienten.
    Notes: Summary Postobstructive diuresis occurs after relief of bilateral ureteral obstruction despite the persistent decrease in renal cortical perfusion and glomerular filtration rate (GFR). After an initial transient rise in renal blood flow (RBF) during acute ureteral obstruction, tubular damage and progressive vasoconstriction with decreased RBF, especially of medullary perfusion, are observed with chronic obstruction. These are associated with an activation of the renin-angiotensin system and of renal prostaglandin (PG) synthesis with enhanced production of the vasoconstrictor thromboxane A2. Azotemia and extracellular fluid volume (ECFV) expansion result from impaired renal function. Mechanisms of polyuria following relief from bilateral chronic obstruction include enhanced PGE-mediated medullary blood flow, structural and functional tubular damage with decreased sodium reabsorption and (vasopressin-resistent) impaired renal concentrating ability, osmotic diuresis, activation of natriuretic factors following ECFV-expansion, and sometimes iatrogenic excessive fluid replacement. The resulting loss of fluid and electrolytes represents a major hazard in patients after surgical correction of congenital or acquired urinary tract obstruction.
    Type of Medium: Electronic Resource
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