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  • 1
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 34 (1956), S. 765-767 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 34 (1956), S. 163-166 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 37 (1959), S. 774-779 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1440
    Keywords: Atrial pacing ; coronary artery disease ; ECG ; hemodynamics ; stress testing ; Angina pectoris ; Coronarinsuffizienz ; Belastungstest ; EKG ; Kreislaufphysiologie ; Vorhofschrittmacher
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Vergleichende hämodynamische Untersuchungen wurden bei 38 Coronarkranken und ebensoviclen Herzgesunden aus einer Gruppe von 143 Untersuchungen mittels kontrollierter Herzfrequenzsteigerung angestellt. Schon bei Ruhe zeigten die Coronarkranken im Durchschnitt eine niedrigere Förderleistung des Herzens bei gleichem oder gar niedrigerem Füllungsdruck des Herzens und vergleichbarem arteriellem und pulmonal-arteriellem Druck. Das hypokinetische Syndrom war außerdem durch einen erhöhten peripheren Gefäßwiderstand gekennzeichnet. Bei der stufenweisen Erhöhung der Herzfrequenz sank der Füllungsdruck des rechten und des linken Herzens, um erst bei höheren Frequenzen wieder anzusteigen. Diese Drucksenkung war bei Coronarkranken weniger ausgeprägt. Während SVI und MSERI sanken, blieben Herzindex und TPR bei allen geprüften Herzfrequenzen unverändert, ebenso die arteriellen und pulmonal-arteriellen Drucke. Die Herzarbeit stieg bei den Coronarkranken etwas an. Die sonst eine Sinustachykardie begleitende Sympathicusaktivierung blieb aus. Infolgedessen wurde die AV-Überleitungszeit zunehmend länger. Dadurch entwickelte sich sehr rasch eine Vorhofpfropfung, in deren Verlauf die Überhöhung dera-Welle besonners bei den Coronarkranken auffiel. — Die Dauer der mechanischen Systole nahm mit steigender Herzfrequenz ab. Bei Coronarkranken war diese Verkürzung weniger ausgeprägt. Das Phänomen der relativ zu langen Systole wird auf eine gestörte Kontraktionsmechanik zurückgeführt. Bei 18 von 38 Patienten wurde ein pectanginöser Anfall durch die „Belastung“ ausgelöst. Die eintretenden hämodynamischen Veränderungen waren denjenigen im ergometrisch induzierten Anfall ähnlich, wahrscheinlich bedingt durch sekundäre Sympathicusaktivierung. Das Verfahren der kontrollierten Herzfrequenzsteigerung erlaubt eine präzise und reproduzierbare Bestimmung der „Angina pectoris-Schwelle“. Die Methode ist sehr schonend und birgt sicher mancherlei noch ungenutzte, diagnostische und therapeutische Vorteile.
    Notes: Summary 38 patients with coronary artery disease and 38 control subjects out of a group of 143 patients examined with the atrial pacing technique underwent a hemodynamic study. Even at rest coronary patients exhibited lower cardiac output, while filling pressures and arterial as well as pulmonary arterial pressures were identical. The hypokinetic syndrome was furthermore characterized by elevated total peripheral resistance in the coronary patients. Atrial pacing initially led to a fall of right and left heart filling pressures. At higher rates this pressure rose definitely above normal in the coronary group, and particularly so if angina pectoris was present, or after sudden cessation of pacing. While cardiac index and TPR remained unchanged within the range of heart rates tested, cardiac work increased slightly in the coronary group. These cases required higher ventricular filling pressures to maintain cardiac output. Progressive prolongation of the PR-interval led to the development of gianta-waves in the right and probably also the left atrial pressure pulse. The height of thea-wave was conspicously exaggerated in the coronary disease group. Left ventricular ejection time shortened progessively with rising heart rate. However, this was not observed in the diseased group. Here, a relative prolongation of the duration of mechanical systole was observed and interpreted as evidence of altered contractile properties of the ischemic myocardium. 18 of 38 patients developed angina pectoris during atrial pacing. Hemodynamic changes in this group resmbled those in exercise-induced angina, the reason being most likely a secondary activation of the sympathetic system. Atrial pacing provides a precise and reproducible means for determination of the angina threshold. The hemodynamic alterations, however, appear to be fundamentally different of those occuring in spontaneous or exercise-induced angina. Diagnostic and therapeutic potentials of the atrial pacing method appear considerable, yet they are largely unexplored.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1238
    Keywords: Transthoracic electrical impedance ; Acute respiratory failure ; Pulmonary interstitial edema ; Intrathoracic fluid volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The alteration (ΔZ 0 ) of transthoracic electrical impedance (TEI) during extracorporeal hemodialysis (EHD) was investigated in two Groups of patients with acute renal and acute respiratory failure, that differed with respect to the severity of respiratory insufficiency. Group I had moderate respiratory failure (Fi O 2 0.31±0.10, Pa 0 2 84±14 mmHg), and Group II had severe respiratory failure (Fi 0 2 0.75±0.17, Pa O O 77±14 mmHg). There was a significant correlation between increase in TEI (ΔZ0) and decrease in body weight (ΔBW) in each individual patient, but the slope of regression lines was remarkably flattened in Group II. In Group I, ΔTEI was 1.9±0.9 Ω, the calculated TEI for 500 gr decrease in BW (ΔZ0–500 gr) was 0.59±0.21 Ω, and a significant correlation existed between pooled data of ΔZ0 and ΔBW. In Group II TEI increased less significantly, ΔTEI was 0.6±0.3 Ω (P〈0.001), ΔZ0–500 gr was 0.26±0.27 Ω (P〈0.01), and there was no correlation between pooled data of ΔZ0 and ΔBW. Increase of TEI in Group II could be completely attributed to increase in hematocrit. It is concluded that patients of Group I with acute renal failure and moderate respiratory failure lost intrathoracic fluid during EHD, whereas patients of Group II with severe respiratory failure did not. TEI during EHD may serve as a test for detection of fixed fluid within the pulmonary interstitium indicating a poor prognosis of the acute respiratory failure.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 7 (1981), S. 77-87 
    ISSN: 1432-1238
    Keywords: Burn toxins ; Immunotherapy ; Liver damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Modern intensive care combined with current improvements in the specific, systemic and local therapy of burns has delayed the mortal effects of severe burns. Nor has there been any significant improvement in this mortality during the last decade. The occurrence of uncontrollable infection and sepsis due to gram-negative bacteria or fungi as the basic cause of death was not a satisfactory explanation. So, progress should only be expected from a new concept in burn treatment. This new concept should be to view the burn disease as being caused by toxic factors induced by thermal injury to the skin. Electron-microscope studies in mice and rats have revealed similar mitochondrial alterations in hepatocytes after either a sublethal controlled burn injury or an intraperiotoneal application of an equivalent dose, of a cutaneous burn toxin. The intraperitoneal injection of different amounts of the burn toxin indicated, that the extent of the mitochondrial changes correlated directly with the dose of toxin. Investigations of liver metabolism suggested an inhibition of the oxygenation chain. The incubation of isolated liver cells together with the burn toxin demonstrated by scanning electron microscopy a direct cytotoxic effect of the burn toxin. In animal tests the pathogenic effect of the burn toxin could be prevented by treatment with an antitoxic IgG generated in sheep. The fatal sepsis of severely burned patients is the consequence of a decreased host defence against infections, which is caused by a primary and general toxic alteration of the whole organism. One important aspect of treatment should therefore be the elimination of burn toxins. To achieve this management should include primary excision of the burns, local application of nonabsorbable protein-complex-binding substances and specific passive immuno-therapy with an antitoxic IgG.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-2451
    Keywords: Isolated rat hepatocytes ; Burnt skin ; Toxic effect of a burn toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Existenz von bei der Verbrennung in der Haut entstehenden toxischen Substanzen und deren Bedeutung für die Pathogenese der Verbrennungskrankheit wird heute weithin als wahrscheinlich angesehen. In der vorliegenden Arbeit wurde der Stoffwechsel isolierter Hepatocyten sowie deren Ultrastruktur unter dem direkten Einfluß sowie nach systemischer Applikation eines aus verbrannter Menschen- und Mäusehaut isolierten hochgereinigten toxischen Faktors untersucht. Unbehandelte Zellen sowie solche, die mit der physiologischen, nicht toxischen Vorstufe des Toxins behandelt wurden, dienten als Kontrolle. Direkt mit dem Toxin inkubierte Zellen wiesen keine Veränderung der Gluconeogenese, eine deutliche Verringerung der Harnstoffsynthese und eine noch deutlichere Reduktion der Glykogenbildung aus den meisten der angebotenen Prekursoren auf. Rasterelektronenmikroskopisch fanden sich deutliche Schädigungen der Zelloberfläche. Zellen von zuvor mit Toxin behandelten Tieren zeigten Einschränkungen aller Syntheseleistungen und wesentlich geringere Membranschäden. Ein direkter zelltoxischer Effekt des Toxins konnte somit gezeigt werden.
    Notes: Summary The existence of a burn toxin which could be responsible for the late burn disease has become increasingly accepted. The present study investigates both metabolism and ultrastructure of isolated rat hepatocytes both under the influence of a burn toxin isolated from burnt mouse and human skin and of its native nontoxic precursor. Cells from rats treated with toxin systematically were also investigated. The cells directly incubated with toxin showed no alterations of gluconeogenesis, but a reduced urea — and glycogensynthesis from most precursors used. Cells of pretreated rats were reduced in all functions and showed more distinct ultrastructural damage, while those incubated directly were significantly more altered. The results prove a direct toxic effect of a burn toxin on isolated liver cells.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 33 (1955), S. 678-688 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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