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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 29 (1937), S. 394-397 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  131. Kongress der Deutschen Gesellschaft für Chirurgie; 20140325-20140328; Berlin; DOC14dgch534 /20140321/
    Publication Date: 2014-03-25
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  17. Grazer Konferenz - Qualität der Lehre 2013: Teaching medical skills; 20130404-20130406; Wien, Österreich; DOCW02c /20131129/
    Publication Date: 2013-11-30
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  17. Grazer Konferenz - Qualität der Lehre 2013: Teaching medical skills; 20130404-20130406; Wien, Österreich; DOCP18 /20131129/
    Publication Date: 2013-11-30
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  46. Jahrestagung der Deutschen Gesellschaft der Plastischen, Rekonstruktiven und Ästhetischen Chirurgen (DGPRÄC), 20. Jahrestagung der Vereinigung der Deutschen Ästhetisch-Plastischen Chirurgen (VDÄPC); 20151001-20151003; Berlin; DOC023 /20150928/
    Publication Date: 2015-09-29
    Keywords: reconstructive microsurgery ; elderly ; free flap transfer ; ddc: 610
    Language: English
    Type: conferenceObject
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  • 6
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2013); 20131022-20131025; Berlin; DOCPO13-982 /20131023/
    Publication Date: 2013-10-24
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 7
    ISSN: 1435-1803
    Keywords: Free radicals ; spin trapping ; infarct size ; reperfusion injury ; ischemic cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ischemic, reperfused porcine hearts were used to investigate whether the spin trap agent PBN (N-tert-butyl-alpha-phenylnitrone) attenuates postischemic cell death by scavenging of free radicals. The left anterior descending coronary artery (LAD) was ligated distally in 16 pigs for 45 min and then reperfused for 3 h. PBN (coronary concentration approximately 1 mM) was infused into the LAD of eight pigs during the first 45 min of reperfusion. Electron spin resonance spectroscopy (ESR) was performed to identify free radical adducts in the reperfused coronary venous blood. Regional systolic shortening (SS%) was determined by sonomicrometry. Infarct size was evaluated as the percentage of infarcted (tetrazolium stain) to ischemic (dye technique) myocardium. The transmural ultrastructural degree of myocardial injury as well as myocardial ATP levels were assessed at the end of the experiment. Intracoronary treatment with PBN during early reperfusion did not attenuate myocardial damage. Infarct sizes (control group 59±19%, treated group 55±14%), transmural ultrastructural alterations, myocardial ATP concentrations (control group 1.8±0.3 μmol/mg frozen weight, treated group 1.7±0.4 μmol/mg) and regional systolic shortening at the end of the experiments (control group −1±5%, treated group −2±6% did not differ significantly. Furthermore, under various experimental conditions of spin trapping, free radical adducts could not be identified in coronary venous blood during early reperfusion. The results suggest that the spin trap agent PBN (1 mM) does not affect postischemic cell death in porcine hearts.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-1803
    Keywords: infarct size ; reperfusion-inducedarrhythmias ; oxygen free radicals ; superoxide dismutase ; porcine hearts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of recombinant human superoxide dismutase (rh-SOD) on infarct size was investigated in porcine hearts. The left anterior descending coronary artery was occluded in each of 24 anesthetized pigs for 45 min and reperfused for 24 h. The animals were randomly assigned to either rh-SOD (n=12) or placebo treatment (n=12). 2 min before reperfusion, an intracoronary (i.c.) infusion of rh-SOD (total dose: 2000 U/kg) or placebo was started which lasted for up to 45 min reperfusion. At the end of the experiment, the infarcted myocardium was assessed using a tetrazolium stain (NBT) and related to the risk region which was determined with a fluorescent dye. Two pigs of the SOD group and one of the control group died before the end of the experiments. Except for a lower calculated myocardial oxygen consumption and a lower dp/dtmax in the SOD group during ischemia, hemodynamic parameters of the two groups did not differ significantly. rh-SOD i.c. treatment during reperfusion did not reduce infarct size significantly. Infarct size amounted to 74±13% in the control group and to 66±19% in the treated group. The incidence of reperfusion arrhythmias was not affected by rh-SOD treatment. It is concluded that i.c. rh-SOD treatment at the beginning of reperfusion neither significantly reduces infarct size nor diminishes the incidence of reperfusion arrhythmias in this preparation.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-1803
    Keywords: infarction ; tetrazolium staining ; regionalmyocardial function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The temporal development of infarcts was histochemically and functionally determined in porcine hearts. In one series of experiments (22 pigs), the distal third of the left anterior descending coronary artery (LAD) was transiently occluded for periods between 20 and 90 min and was reperfused for another 24h. At the end of the experiments, the infarcted myocardium of four tissue slices was determined with a tetrazolium stain and related to the risk region which was delineated by a fluorescent dye. Infarcts started to develop in the ischemic septum and the subendocardial layer of the free anterior wall between 20 and 35 min of ischemia. Thereafter, infarctions progressed rapidly from the inner towards the outer layer at risk. The jeopardized anterior left ventricular wall became almost completely infarcted within 60 min of ischemia. In a second series of experiments (10 pigs) recovery of systolic shortening was studied with implanted ultrasonic crystals over 3 weeks of reperfusion. At the end of the experiments, systolic shortening was about 75% of baseline level when ischemia had lasted between 20 and 35 min. Almost no recovery was observed when the occlusion time lasted 45 to 60 min. This study suggests that the assessment of myocardial infarction with a tetrazolium stain after 24 h of reperfusion corresponds very well with functional recovery after 3 weeks of reperfusion. Furthermore, determination of regional myocardial function of the ischemic, reperfused segment in the chronic stage may be considered an additional tool to evaluate therapeutic effects on infarct size in this model.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1435-1803
    Keywords: NAD ; ultrastructure ; ischemic cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der biochemische Mechanismus, der dafür verantwortlich ist, daß reversibel geschädigte Zellen schließlich sterben, ist unbekannt. Wir untersuchten, ob der Verlust an Nicotinamidcoenzymen der entscheidende Grund für den Zelluntergang sein kann. Bei 6 Hunden wurde der Ramus interventricularis anterior für 4 h unterbunden. Transmurale Nadelbiopsien wurden nach 1/2 h, 1 h, 1 1/2 h, 2 h und 4 h Ischämie aus dem ischämischen Gebiet entnommen und in subepikardiale und subendokardiale Hälften unterteilt. Zu den angegebenen Zeiten wurden die Konzentrationen der Coenzyme NAD, NADH und NADPH in den Biopsien gemessen und der Schädigungsgrad des Gewebes durch elektronenmikroskopische Untersuchung bestimmt. Die Glycohydrolaseaktivität (E.C. 3.2.2.5) wurde in Gehirn, Herz, Niere und Skelettmuskel von 4 Ratten ermittelt. Gesamt-NAD, die Summe von NAD und NADH, nahm signifikant nach einer Stunde im ischämischen Subendokard ab. Der Verlust and NADPH trat erst nach zwei Stunden ein. Wenn durch ultrastrukturelle Untersuchung irreversible Zellschädigung festgestellt wurde, hatte der Gesamtgehalt von NAD etwa 60–70% abgenommen. Die Glycohydrolaseaktivität war am höchsten im Gehirn, gefolgt von Herz, Niere und Skelettmuskel und entspricht der unterschiedlichen Ischämietoleranz dieser Organe. Wir nehmen an, daß der entscheidende Grund für die irreversible Zellschädigung die Gewebsazidose ist, die zu einer Aktivierung der Glycohydrolase führt, die ihrerseits die lebenswichtigen Coenzyme spaltet.
    Notes: Summary We investigated if the loss of nicotinamide coenzymes in ischemic-infarcted myocardium may be responsible for the transition from reversibly ischemic to irreversibly infarcted cell damage. The LAD was occluded in 6 dogs for 4 h. Transmural needle biopsies were taken from the ischemic-infarcted region after 1/2, 1, 1 1/2, 2, and 4 h of ischemia and further divided into subepicardial and subendocardial halves. At each time interval the concentration of the nicotinamide coenzymes NAD, NADH, and NADPH were measured, and the degree of cellular injury was evaluated by electron microscopy. The glycohydrolase activity (EC 3.2.2.5), the enzyme which splits NAD, was determined in brain, myocardium, kidney, and skeletal muscle of 4 rats. Total NAD, the sum of NAD and NADH, started to decrease significantly in the ischemic subendocarium 1 h after onset of ischemia. Degradation of NADPH occurred later. Loss ot total NAD was about 60–70% when electron microscopy diagnosed irreversible cell injury. The glycohydrolase activity was the highest in brain followed by myocardium, kidney, and skeletal muscle, reflecting the different tolerances of these tissues towards ischemia. The key mechanism for ischemic injury seems to be the tissue acidosis which activates the glycohydrolase leading to a loss of the vital coenzymes.
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