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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 54 (1976), S. 323-332 
    ISSN: 1432-1440
    Keywords: Pulmonary gas exchange during exercise ; Myocardial infarction ; Late period of recovery ; Pulmonaler Gaswechsel unter Belastung ; Myokardinfarkt ; Späte Rehabilitationsphase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In der späten Rehabilitationsphase nach Myokardinfarkt (13–24 Monate p. infarctum) wurde der pulmonale Gaswechsel neben hämodynamischen Parametern bei 23 Patienten unter Belastung untersucht. Der Belastungsverlauf der gemessenen Parameter gleicht dem Herz- und Lungengesunder. Die arteriellen Blutgaspartialdrucke ( $$Pa_{O2} , Pa_{CO2} $$ ) bleiben gegenüber den Ruhewerten unverändert oder zeigen nur geringe statistisch nicht signifikante Änderungen. Die alveoläre Ventilation $$\dot V_A $$ zeigt im Belastungsverlauf bei allen Patienten keine Unterschiede. Herzzeitvolumen $$\dot Q$$ , Atemminutenvolumen $$\dot V_E $$ , die Toträume, alveolo-arterielle Partialdruckdifferenzen der Atemgase ( $$AaD_{O_2 } , aAD_{CO_2 } $$ ) und Ventilations-Perfusionsverhältnis der Gesamtlunge $$\dot V_A /\dot Q$$ lassen jedoch erkennen, daß entsprechend der unterschiedlichen Arbeitskapazität der Patienten diese Parameter einen differenten Belastungsgang zeigen. Da sich die unterschiedliche Arbeitskapazität nach dem Verhalten von Herzzeitvolumen $$\dot Q$$ und gemischtvenösen Blutgaspartialdrucken aus der verschiedenen kardialen Funktion der Patienten erklären läßt, erscheint die Pathologie des pulmonalen Gaswechsels von der jeweiligen linksventriculären Funktion des Patienten abhängig. 12 der 23 untersuchten Patienten, die nach hämodynamischen Kriterien eine Belastungsinsuffizienz des Herzens zeigten, wiesen die ausgeprägtesten Änderungen des pulmonalen Gaswechsels auf. Die unterschiedliche Arbeitskapazität der Patienten ist allein von der kardialen Funktion begrenzt. Eine Leistungslimitierung durch Störung der Lungenfunktion ließ sich nicht beweisen.
    Notes: Summary After myocardial infarction in the late period of recovery (13–25 months p. infarctum) pulmonary gas exchange in 23 patients was measured besides as hemodynamic parameters during exercise. The parameters take a course similar to that of subjects without lung and heart diseases. Arterial blood gas tensions ( $$Pa_{O_2 } ,Pa_{CO_2 } $$ ) remain unchanged compared to resting values. Alveolar ventilation did show no difference in any of the patients. Minute ventilation $$\dot V_E $$ , the various dead spaces, alveolar-arterial gas differences ( $$AaD_{O_2 } , aAD_{CO_2 } $$ ) and ventilation-perfusion ratios of the whole lung $$\dot V_A /\dot Q$$ suggest however that these parameters show different courses according to the physical capacity of the patients. As the physical capacity of each patient is due to different cardiac functions taken by cardiac output and mixed venous blood gas tensions alterations of pulmonary gas exchange seemed to be dependent on the respective left ventricular function of the heart. Of the twenty-three patients, twelve with cardiac failure under exercise showed the most pronounced alterations in pulmonary gas exchange. Therefore, the different physical work capacity of the patients are determined only by cardiac function. No limitation of the productivity due to impeded lung function could be proved.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 64 (1986), S. 301-306 
    ISSN: 1432-1440
    Keywords: Myocardial infarction ; Fibrinolysis ; Plasminogen activators
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The early treatment of acute myocardial infarction has changed rapidly in recent years. Given the fact that an occlusive coronary thrombus can be found in most infarct patients within 4 h after clinical symptoms, the idea of instituting medical or mechanical recanalization of the occluded vessel is intriguing. However, invasive measures are time consuming, expensive and not freely available to a great number of patients. Thus, only i.v. fibrinolytic therapy of acute myocardial infarction will gain wider application in the near future. Several concepts have been worked out, one of which uses a high-dosage streptokinase or urokinase regimen. A different therapeutic alternative has been made possible by the development of selective fibrinolytic substances, such as the tissue-type plasminogen activator (t-PA) or the anisoylated plasminogen-streptokinase activator complex (APSAC). Preliminary clinical data have shown that the coronary artery patency rate achieved after i.v. administration of t-PA or APSAC is higher than that after conventional treatment with streptokinase or urokinase. The incidence of severe bleeding complications is low and comparable in these studies. However, until myocardial salvage has been demonstrated with early i.v. fibrinolytic therapy in acute myocardial infarction in a placebo-controlled randomized trial, this therapeutic concept will still be unsettled.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Myocardial infarction ; Late recovery period ; Cardio-pulmonary data at rest and during exercise ; Myokardinfarkt ; Späte Rehabilitationsphase ; Kardio-pulmonale Funktionsparameter in Ruhe und unter Belastung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 22 Patienten, die 1–2 Jahre zuvor komplikationslos einen Myokardinfarkt durchgemacht hatten, wurden bis an die Grenze ihrer Leistungsfähigkeit stufenweise ergometrisch belastet. Entsprechend der Belastbarkeit wurden die Patienten in vier Leistungsgruppen eingeteilt und die Anpassung der wichtigsten kardio-pulmonalen Funktionsparameter in jeder Gruppe getrennt verfolgt. Dabei waren in der Hälfte der Fälle bereits in Ruhe diskrete Insuffizienzzeichen nachweisbar. Bei der folgenden Ergometerbelastung stellten sich auch bei den übrigen Patienten in der ersten Belastungsstufe Insuffizienzzeichen ein.
    Notes: Summary From 22 patients in the late period of recovery from myocardial infarction, cardio-pulmonary data were recorded at rest and during exercise. The physical work was increased stepwise until patients reached their individual limit of exercise. According to the different work capacity four groups of patients were formed with the aim to demonstrate the adaption processes of cardio-pulmonary parameters until reaching the peak of work capacity. In one half of the patients we still found signs of cardial insufficiency at rest. After only slight physical work signs of cardiac insufficiency appeared also in the other half of patients.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-1803
    Keywords: atrial natriuretic peptide ; heart failure ; regionalblood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 μg bolus followed by continuous infusion of 1.0 μg/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular enddiastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p〈0.01), and increased 5–10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 92 (1997), S. 87-93 
    ISSN: 1435-1803
    Keywords: Calcium ; heart failure ; sarcoplasmic reticulum ; geneexpression ; human myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is accumulating evidence that disturbed calcium homeostasis may play a key role in the pathophysiology of human heart failure. Because disturbed calcium handling could result from altered protein expression, levels of calcium handling proteins were quantitated by Western Blot analysis in failing and nonfailing human myocardium from hearts with endstage failing dilated or ischemic cardiomyopathy. Protein levels of the sarcoplasmic reticulum calcium release channel (ryanodine receptor) and of calcium storage proteins (calsequestrin and calreticulin) were similar in failing and nonfailing human myocardium. However, proteins involved in calcium removal from the cytosol were significantly altered in the failing human heart: 1) SR-Ca2+-ATPase, relevant for removal of calcium from the cytosol into the lumen of the sarcoplasmic reticulum, was decreased; 2) phospholamban, which inhibits the SR-Ca2+-ATPase in the basal unphosphorylated state, was slightly decreased; 3) the ratio of SR-Ca2+-ATPase to phospholamban was decreased; 4) the sarcolemmal Na+−Ca2+-exchanger, relevant for transsarcolemmal calcium extrusion was increased in the failing hearts. In summary, altered levels of proteins involved in calcium removal from the cytosol suggest an increase in transsarcolemmal calcium elimination relative to sarcoplasmic reticulum calcium removal. These findings support the concept that reduced function of the sarcoplasmic reticulum to accumulate calcium may reflect a major defect in excitationcontraction coupling in human heart failure.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 91 (1996), S. 17-22 
    ISSN: 1435-1803
    Keywords: Excitation-contraction coupling ; heart failure ; force-frequency relation ; calcium cycling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Myocardial function, intracellular calcium and levels of calcium cycling proteins were analyzed in failing and nonfailing human myocardium. Myocardial function was evaluated by the isometric force-frequency relation, and intracellular calcium was studied by aequorin light emission. When stimulation frequency was increased above 30 min−1, there was a continuous increase in isometric tension development in the nonfailing myocardium. In contrast, in failing myocardium, frequency potentiation of contractile force was blunted or inverse. As a consequence, at higher rates of stimulation, twitch tension was reduced significantly in failing compared to nonfailing human myocardium. Aequorin measurements indicated that the contractile deficit in the failing myocardium at higher rates of stimulation is associated with decreased free intracellular calcium concentration. Western blot analysis indicated that in the failing myocardium protein levels of SR-Ca2+-ATPase are significantly reduced and protein levels of Na+−Ca2+-exchanger are significantly increased. Levels of phospholamban are slightly reduced in the failing myocardium, and ryanodine receptor and calsequestrin protein levels are unchanged. There was a close positive correlation between the protein levels of SR-Ca2+-ATPase and frequency potentiation of contractile force. From these data, we conclude that in failing compared to nonfailing human myocardium 1) force-frequency relation is blunted or inverse. 2) Frequency-dependence of contractile force is closely correlated with frequency-dependence of intracellular calcium cycling. 3) Protein levels of SR-Ca2+-ATPase may determine frequency-dependence of sarcoplasmic reticulum calcium release. 4) Calcium elimination by an increased number of Na+−Ca2+-exchanger molecules may be a compensatory mechanism to prevent diastolic calcium accumulation in failing myocardium with a reduced number of SR calcium pumps.
    Type of Medium: Electronic Resource
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