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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 19 (1987), S. S53 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Primary hypercholesterolemia ; HMG CoA reductase inhibition ; Steroid hormones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the effect of a 16 week therapy with the HMG CoA reductase inhibitor lovastatin in 29 patients (mean age 43 years) with primary hypercholesterolemia. All patients had cholesterol levels above 250 mg/dl (mean 348 ±96 mg/dl) inspite of a lipid lowering diet and a therapy with conventional lipid lowering drugs during a three month screening period. After 4 weeks on placebo 20 mg lovastatin was given orally for 4 weeks. If total cholesterol exceeded 200 mg/dl the dose of lovastatin was increased monthly by 20 mg up to the maximal dose of 80mg/day. After 16 weeks lipid values changed compared with the placebo period: total-cholesterol −25%, triglycerides −8.6%, LDL-cholesterol −31%, APO B −25%, HDL-cholesterol +5.8%, APO AI +0.8%, total-cholesterol/HDL-cholesterol −25%. There was a significant improvement of lipid parameters after lovastatin therapy compared with conventional lipid lowering drugs at the end of the screening period. Lovastatin was well tolerated. A small and reversible rise of transaminases and/or creatinine kinase was observed in 6 patients. Basal levels of ACTH in the morning increased significantly during lovastatin therapy within the normal range. This observation was more frequent in females (10/12) than in males (10/ 17).
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 68 (1990), S. 1201-1201 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 144-144 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 58 (1980), S. 219-225 
    ISSN: 1432-1440
    Keywords: Autoantikörper ; Antisarkolemmale Antikörper ; Antiendotheliale Antikörper ; Antimyokardiale Antikörper ; Immunsuppressive Serumfaktoren ; Seruminhibitionsfaktoren ; Akute und chronische Myokarditis ; Viruserkrankungen ; Autoantibodies ; Antisarcolemmal antibodies ; Antiendothelial antibodies ; Antimyocardial antibodies ; Immunosuppressive serum factors ; Serum inhibition factors ; Acute and chronic myocarditis ; Viral diseases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 54 patients with acute and “chronic” myocarditis were tested for autoantibodies and serum inhibition factors. 11 patients had a viral myocarditis, 17 a “chronic” myocarditis. By comparing the antibody pattern of sera of patients with defined viral myocarditis with those of patients with myocarditis of unknown etiology we could demonstrate that antisarcolemmal (ASA) and antiendothelial antibodies (AEA) are markers of a viral involvement in heart disease. 10 of the 11 patients with Coxsackie B and Influenza virus myocarditis demonstrated this pattern. 15 out of 26 patients with undefined myocarditis showed the same antibody pattern, in sera of 17 patients with features suggestive of “chronic” myocarditis antiendothelial and antisarcolemmal antibodies occurred less frequently. The latter patients showed antinuclear antibodies in 65% with titres up to 1:40. Whereas SIF could be demonstrated in all patients with acute viral myocarditis, and in 11 out of 26 patients with acute undefined myocarditis in the early period and only in 3 patients with “chronic” myocarditis, SIF persisted in these 3 patients with chronic myocarditis in whom we suspected an autoimmune process. Our investigation demonstrates that an etiological classification of undefined myocarditis can be obtained by serological markers and that serum inhibition factors occur transiently in acute and continuously in autoimmune myocarditis.
    Notes: Zusammenfassung 54 Patienten mit akuter und chronischer Myokarditis wurden auf Antikörper und Seruminhibitionsfaktoren untersucht. Bei 11 Patienten konnte eine Virusätiologie gesichert werden, bei 17 Patienten bestand der Verdacht auf eine „chronische“ Myokarditis. Aus dem Vergleich der Antikörpermuster zwischen Patienten mit bekannter Virusätiologie und ätiologisch nicht definierter Myokarditis konnte gefolgert werden, daß vor allem Antikörper gegen Sarkolemm und Gefäßendothel Marker eines virusinduzierten Prozesses am Myokard sind. 10 der 11 Patienten mit Influenza, Coxsackie B3-und Coxsackie B4-Myokarditis hatten diese Konstellation. 15 der 26 Patienten mit ätiologisch unklarer Myokarditis wiesen dasselbe Antikörpermuster auf, während bei 17 Patienten mit Verdacht auf chronische Myokarditis antiendotheliale Antikörper und antisarkolemmale Antikörper seltener nachweisbar waren. 65% der Patienten mit „chronischer“ Myokarditis wiesen Antikörper gegen Kerne mit einem Titer bis zu 1:40 auf. Während Seruminhibitionsfaktoren (SIF) bei allen Patienten mit akuter Virusmyokarditis und bei 11 von 26 Patienten mit akuter, ätiologisch nicht definierter Myokarditis nachweisbar waren, persistierten sie nur bei 3 Patienten mit chronischer Myokarditis, bei denen aufgrund des Auftretens von antinukleären Faktoren und der fehlenden antiendothelialen und antisarkolemmalen Antikörper ein autoimmuner Prozeß angenommen werden könnte. Die Untersuchungen zeigen, daß eine ätiologische Klassifizierung unklarer Myokarditiden mit serologischen Markern möglich ist und daß Seruminhibitionsfaktoren bei akuten Myokarditiden passager und bei autoimmunen Myokarditiden persistierend vorkommen können.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 988-988 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 185 (1985), S. 429-443 
    ISSN: 1433-8580
    Keywords: Myocardial blood flow ; Angiotensin II ; Saralasin ; Nephrectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen (n = 7). A third group of dogs was ventilated with room air and bilaterally nephrectomized 5 h prior to starting the experimental protocol (n = 7). After control data had been obtained, dogs were bled from the femoral arteries into a pressurized reservoir which maintained blood pressure at 45 ± 1 mm Hg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 µg/kg per min). Coronary blood flow was reduced by hemorrhage, and no significant difference existed in coronary flow during hemorrhage among the three groups. Coronary sinus oxygen saturation was diminished in control animals during hemorrhage from 26% ± 1% to 17% ± 1% (P 〈 0.05) but normal in 100% oxygen ventilated animals (30% ± 3%) and in nephrectomized dogs (34% ± 4%). Coronary oxygen extraction was reduced by saralasin in intact but not in nephrectomized dogs. In six additional experiments, in which blood pressure was not artificially held constant during saralasin infusion, saralasin still significantly improved coronary sinus oxygen saturation and thus reduced coronary oxygen extraction. The data suggest that both hypoxia and the reninangiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0584
    Keywords: Type-IIa hypercholesteremia ; Lovastatin ; Platelet function ; Fibrinogen ; Clotting inhibitors ; Fibrinolytic activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a study of 20 patients with hypercholesterolemia (type IIa) the effects of lovastatin (20–80 mg/ day) on various clotting and thrombosis parameters were monitored for 12 months. On 11 occasions various cholesterol fractions and clotting parameters were determined in each patient. In additon, the clotting inhibitors AT III, protein C, protein S, and C1-esterase inhibitor and the fibrinolysis parameters plasminogen and α2-antiplasmin were examined. Platelet function was monitored on the basis of spontaneous and induced (collagen, ADP, epinephrine, ristocetin) aggregation. Lovastatin in the above dosage brought about a 66 mg/dl (from 320 ± 12.6 to 254 ± 12.0 mg/dl) reduction in the total cholesterol level and a 56 mg/dl (from 244 ± 11.4 to 188 ± 12.1 mg/dl) reduction in LDL cholesterol at the end of the study. Fibrinogen showed a significance decrease during the study period, whereas PT and aPTT remained unaffected. The initial slopes of the ADP-induced platelet aggregation revealed a significant decrease. C-reactive protein and platelet count remained within the normal range, indicating no significant change. Thrombin clotting time, AT III, Cl-esterase inhibitor, plasminogen, and α2-antiplasmin were not modified. Protein C and S behaved in a contradictory way, but remained within the normal range. Long-term treatment with lovastatin was associated with a significant reduction of fibrinogen levels and platelet aggregation induced by ADP in type-IIa hypercholesterolemic patients. These alterations, as well as their role in cardiovascular disease, should be the subject of further investigations.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 42 (1964), S. 1005-1011 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Es wurden röntgenologische Kriterien pulmonaler Drucksteigerung bei venöser Stauung mit den durch Rechtsherzkatheterisierung gemessenen Druckwerten eines größeren Krankengutes von Mitralklappenfehlern verglichen. Dabei fand sich als Frühsymptom der venösen Drucksteigerung und als Hinweis auf die beginnende pulmonale arterielle Hypertonie die Erweiterung der oberen Lungenvenen. Der manifeste pulmonale Hochdruck ging mit einer Erhöhung des Pulmonalsegmentes über 6 mm und mit einer Erweiterung der absteigenden rechten Pulmonalarterie über 16 mm einher. B-Linien fanden sich überwiegend bei höheren Schweregraden venöser Stauung und arterieller Drucksteigerung (oberhalb eines PAP von 25 mm Hg und eines PCPm von 15 mm Hg). Miliare Lungenstauung, Hämosiderose sowie Stauungsfibrose sind Ausdruck eines höheren Schweregrades und Zeichen langjährig bestehender pulmonaler Hypertonie.
    Type of Medium: Electronic Resource
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