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  • 1
    ISSN: 1432-2307
    Keywords: Septic shock ; Skeletal muscle ; Porcine shock model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In domestic pigs, intermitted application ofEscherichia coli-endotoxin was used to create an animal model for a prolonged hypo- and hyperdynamic septic shock-like state and to investigate mechanisms of multiple organ failure. Here, we describe the changes in skeletal muscle after 18 h (2 animals) and 48 h (6 animals) of septic shock. Two pigs for each observation period that received physiologic saline solutions instead of endotoxin served as controls. The earliest lesions were endothelial cell damage with endomysial oedema and swelling of mitochondria in muscle fibres. With increasing degree of endothelial cell damage, pericytes showed degenerative changes with cytoplasmic fragmentation and karyolysis. After 48 h of shock, endomysial oedema was increased with fibrinogen present. Muscle fibre diameters were increased and swollen mitochondria and segmental necrosis of muscle fibres were frequently observed. However, phagocytic reaction or regenerative changes were not detected. In this respect, skeletal muscle lesions in septic shock differ from ischemic damage, which is characterized by early phagocytosis. Tumour necrosis factor alpha (TNFα) was increased greatly and significantly in the serum of the pigs that received endotoxin. The lesions described may be the result of both direct damage to muscle fibres by the endotoxin and/or the increased levels of TNFα and indirect damage because of the increased diffusion distance, due to the endomysial oedema. The loss of blood proteins into the endomysium may also play a role in generating hypoproteinemia in patients with septic shock.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2307
    Keywords: Septic shock ; Skeletal muscle ; Porcine shock model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In domestic pigs, intermitted application of Escherichia coli-endotoxin was used to create an animal model for a prolonged hypo- and hyperdynamic septic shock-like state and to investigate mechanisms of multiple organ failure. Here, we describe the changes in skeletal muscle after 18 h (2 animals) and 48 h (6 animals) of septic shock. Two pigs for each observation period that received physiologic saline solutions instead of endotoxin served as controls. The earliest lesions were endothelial cell damage with endomysial oedema and swelling of mitochondria in muscle fibres. With increasing degree of endothelial cell damage, pericytes showed degenerative changes with cytoplasmic fragmentation and karyolysis. After 48 h of shock, endomysial oedema was increased with fibrinogen present. Muscle fibre diameters were increased and swollen mitochondria and segmental necrosis of muscle fibres were frequently observed. However, phagocytic reaction or regenerative changes were not detected. In this respect, skeletal muscle lesions in septic shock differ from ischemic damage, which is characterized by early phagocytosis. Tumour necrosis factor alpha (TNFα) was increased greatly and significantly in the serum of the pigs that received endotoxin. The lesions described may be the result of both direct damage to muscle fibres by the endotoxin and/or the increased levels of TNFα and indirect damage because of the increased diffusion distance, due to the endomysial oedema. The loss of blood proteins into the endomysium may also play a role in generating hypoproteinemia in patients with septic shock.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2307
    Keywords: Cardiac muscle ; Microvasculature ; Septic shock ; Porcine shock model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The morphology of cardiac muscle was investigated in a porcine model of septic shock, created by intermitted application of Escherichia coli-endotoxin. The earliest lesions, found after 18 h of septic shock, were endothelial cell swelling, marked leucostasis and slight ischaemic alterations of the muscle fibres. At the end point of the experiments, after 48 h, some fibrin thrombi were found associated with more pronounced ischaemic alterations of cardiac muscle cells and some necrotic fibres. Comparing these findings with the severe endothelial and muscle fibre lesions found in skeletal muscle, the endothelial cells of the heart microvasculature, are clearly more resistant to the attack of the endotoxins and mediators liberated in septic shock.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-2451
    Keywords: Septic shock ; Thromboxan A2 ; Prostacyclin ; Interleucin-6 ; ARDS ; Intestinal ischemia ; Intestinal potassium monitoring
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Beschrieben wird ein tierexperimentelles Sepsismodell, das der Problematik chirurgischer Intensivpatienten entspricht. Nach rezidivierender Applikation von E.-coli-Endotoxin W0111:134 unter standardisierten Bedingungen konnten spezifische hämodynamische, biochemische (TNF, TXA2, PG I2, IL-6, PAF) und morphologische Veränderungen (pulmonales Endothel) nachgewiesen werden. Die sepsisinduzierten ARDS-Veränderungen werden mit einer Hochfrequenzdruck-und-flowmessung mit 385 Meßpunkten fiber einem Atemzyklus analysiert. Die Rolle des Darms in der Sepsis wurde mit ionenselektivem Kaliummonitoring vergleichend auf der Mukosa and Serosa untersucht. Jede Endotoxingabe wurde vom Dünndarm mit selektiven Anstiegen der Kaliumaktivität als Ausdruck einer Endotoxin-induzierten relativen Ischämie beantwortet. Das Profil der Oberflächenkaliumwerte korreliert sowohl mit dem „cardiaco output” als auch mit den Prostazyklinspiegeln. Die während der Versuchsdauer kontinuierlich abnehmende Mukosa-Serosa-Kaliumdifferenz kann als Nachweis einer die Sepsis katalysierenden intestinalen Permeabilitätsstörung interpretiert werden.
    Notes: Abstract The study deals with an animal model for the problems of surgical intensive care patients. Following repeated applications of E. coli endotoxin W0111:134 under standard conditions, specific hemodynamic and biochemical (TNF, TXA2, PGI2, IL-6, PAF) and morphological (endothelium of the lung) alterations were detected. ARDS patterns induced by the sepsis were analyzed by high-frequency measurement of pressure and flow (385 measurements per breathing cycle). The role of the intestine in sepsis was investigated by ion-selective monitoring of surface potassium activity comparing mucosa and serosa. Every injection of endotoxin was followed by a selective increase of the potassium activity revealing relative ischemia induced by the endotoxin. The profile of the potassium levels on the surface correlates both with the cardiac output and with the prostacyclin levels. The continuous narrowing of the difference between mucosa and serosa, potassium during the period of investigation can be regarded as evidence for pathologic change in permeability fostering the septic course.
    Type of Medium: Electronic Resource
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