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  • 1
    Electronic Resource
    Electronic Resource
    Role of oxygen radicals in the microcirculatory manifestations of postischemic injury (1991)
    Springer
    Journal of molecular medicine 69 (1991), S. 1050-1055 
    Details
    ISSN: 1432-1440
    Keywords: Ischemia-reperfusion ; Microcirculation ; Oxygen radicals ; Chemoattractants ; PMN-endothelium interaction ; No-reflow ; Reflow-paradox
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reperfusion after transient tissue ischemia constitutes an irrevocable need to preserve tissue viability. However, release of prolonged ischemia will either result in failure of the microcirculation to reperfusion (no-reflow) and thus the prolongation of hypoxia, or in restoration of blood flow resulting in reoxygenation of the inflicted tissue. While ischemia damages the tissue primarily through hypoxia-induced depletion of energy stores, reoxygenation paradoxically contributes to tissue damage through the formation of oxygen radicals, the release of chemoattractant mediators (TNF, IL-1, LTB4), and the activation of circulating polymorphonuclear leukocytes (PMNs). Through the action of chemoattractant mediators and the upregulation of leukocytic (CD11/CD18) and endothelial adhesion receptors (ICAM, GMP-140), activated PMNs adhere to the endothelium, release further chemoattractants and oxygen radicals and undertain a vicious circle, which will ultimately result in further tissue damage. Both theno-reflow phenomenon and the events initiated by reflow — termed herein as thereflow-paradox — contribute to the failure of the nutritive microvascular perfusion and loss of tissue viability following ischemia and reperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01645157
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Quantitative analysis of microcirculatory disorders after prolonged ischemia in skeletal muscle (1988)
    Springer
    Research in experimental medicine 188 (1988), S. 151-165 
    Details
    ISSN: 1433-8580
    Keywords: Microcirculation ; Skeletal muscle ; Ischemia ; Reperfusion injury ; Hemodilution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reperfusion injury following prolonged ischemia is thought to be caused primarily by microvascular failure. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution with Dextran 60 (hct 30%) could improve microvascular perfusion after 4h of pressure-induced ischemia in skeletal muscle. In 28 Syrian golden hamsters (6–8 weeks/60–80 g b. wt.) a dorsal skinfold chamber and permanent arterial and venous catheters were implanted under Nembutal anesthesia (50 mg/kg b. wt.). Following a recovery period of 48 h pressure-induced ischemia was applied to the skeletal muscle within the skinfold chamber by means of a transparent stamp. Quantitative analyses of microhemodynamics were performed in the awake animal prior to and 15 min, 1, 2, 4 and 24 h after ischemia using vital fluorescence microscopy. In non-treated animals, functional capillary density decreased after 4 h of ischemia to 30% of the initial values (P 〈 0.001); after 24-h reperfusion only 50% of the initially perfused capillaries were reperfused (P 〈 0.001). The heterogeneity of functional capillary density increased after ischemia to a maximum of 2.19 ± 0.94 as compared to 0.48 ± 0.11 prior to ischemia. Capillary RBC-velocity suffered a marked reduction in the early reperfusion phase and did not recover up to the 24-h observation time. In contrast, prophylactic isovolemic hemodilution was associated with only a small and reversible reduction of functional capillary density after 4-h ischemia. At 24-h reperfusion 90% of the initially perfused capillaries were reperfused. Capillary RBC-velocity was reduced in the early reperfusion phase, but returned to normal values within 24h. Thus, prophylactic isovolemic hemodilution resulted in a marked reduction of microvascular reperfusion failure in skeletal muscle. A hematocrit lower than normal prior to ischemia provides better conditions for capillary reperfusion after prolonged ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852316
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Exocrine, but not endocrine, tissue is susceptible to microvascular ischemia/reperfusion injury following pancreas transplantation in the rat (1999)
    Springer
    Transplant international 12 (1999), S. 50-55 
    Details
    ISSN: 1432-2277
    Keywords: Key words pancreas transplantation ; rat ; exocrine tissue ; reperfusion ; Endocrine tissue ; reperfusion ; Microcirculation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract While post-transplant pancreatitis is still a frequently occurring complication of whole pancreas transplantation, dysfunction of the endocrine tissue is rarely observed. Given that microcirculatory disorders play a major role in the pathogenesis of pancreatitis, we hypothesized a dissociation of endocrine and exocrine microvascular control in pancreas transplantation (cold ischemia-reperfusion) and studied this dissociation quantitatively, analyzing the pancreatic microcirculation after heterotopic isogeneic pancreaticoduodenal transplantation in rats by means of fluorescence microscopy. Functional capillary density (FCD) of both exocrine and endocrine tissue of pancreatic grafts after 1 h of cold storage in HTK solution did not differ when compared to sham-operated, time-matched controls. Intermittent capillary perfusion, which is absent under sham control conditions and which is proposed to be operative as a compensatory mechanism to counteract malperfusion, was observed in 52 % of the exocrine, but in only 8 % of the endocrine, tissue studied (p 〈 0.05). In contrast, cold storage of pancreatic grafts for 6 h in HTK resulted in a complete loss of intermittent capillary perfusion in exocrine tissue and, consequently, marked exocrine perfusion failure (decrease in FCD), while FCD of pancreatic endocrine tissue was preserved without any significant change in the incidence of intermittent capillary perfusion. Thus, our results indicate a higher susceptibility of the exocrine pancreas to cold ischemia/reperfusion events that is associated with significant alterations in nutritive perfusion and, thus, with limitations of the oxygen supply to the tissue. This may lead to inflammatory tissue reactions in the clinical setting of pancreas transplantation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050184
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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