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  • Electronic Resource  (2)
  • 2005-2009
  • 1985-1989  (2)
  • 1989  (2)
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  • Electronic Resource  (2)
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  • 2005-2009
  • 1985-1989  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 27 (1989), S. 435-437 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Early ischemic colitis was induced in rats to evaluate the roles of FRs and intraluminal content. After 30 minutes of ischemia, biopsies for histology, conjugated dienes (CD) and malonaldehyde (M), presumptive marker of lipid peroxidation, were obtained at 0, 30, and 60 minutes reperfusion. Histology was unchanged. CD and M were elevated in ischemic and saline controls, and rose progressively during reperfusion; CD and M were essentially the same as non-ischemic controls during reperfusion with intraluminal corticosteroid (c) and Alcide (A). These agents may be beneficial in early ischemic colitis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: heart ; myocardial preservation ; nicotinic acid ; ischemia ; reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cardioprotective effects of an antilipolytic compound, nicotinic acid, on arrested-reperfused myocardium were investigated in the isolatedin situ pig heart preparation. Hearts were preperfused for 15 min in the presence of (5-3H)-glucose and (U-14C)-palmitic acid. Half of the hearts were then perfused with 0.08 mM nicotinic acid for an additional 15-min period, while the remaining control hearts received unmodified perfusion. Arrest was then induced in all animals for 2 h using hypothermic K+ cardioplegia, followed by 60 min of normothermic reperfusion. In control hearts, there were significantly greater levels of long-chain acyl Co-A and acyl carnitine and lower levels of membrane phospholipids than in the nicotinic acid group. While nicotinic acid inhibited β-oxidation during pre-ischemia and reperfusion, it also prevented the degradation of membrane phospholipids. The net result was a reduction of free fatty acid accumulation during arrest and reperfusion in the nicotinic acid group. Glycolysis, as reflected in3H2O production, was significantly increased by nicotinic acid administration. In the control heart as compared to the nicotinic acid group, the incorporation of14C-label from palmitate into triglyceride and cholesterol during arrest was enhanced, while incorporation into phospholipids was depressed. The cardioprotective effects of nicotinic acid were demonstrated by decreased release of creatine kinase and improved coronary blood flow, and cardiac contractility in the reperfused myocardium supplemented with nicotinic acid compared to the control group. These results suggest that nicotinic acid significantly protects the arrested-reperfused myocardium by a) preventing elevation of myocardial fatty acid levels, b) stimulating glycolysis by limiting fatty acid oxidation, c) inhibiting degradation of membrane phospholipids, and d) preventing accumulation of fatty acid metabolites with harmful detergent properties.
    Type of Medium: Electronic Resource
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