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  • 1
    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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  • 2
    ISSN: 1435-1803
    Keywords: ischemia ; reperfusioninjury ; ibuprofen ; prostaglandins ; neutrophils
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The efficacy of using a nonsteroidal anti-inflammatory agent such as ibuprofen for the salvage of ischemic and reperfused myocardium was investigated by examining its ability to improve global and regional functions as well as to preserve high-energy phosphate compounds and inhibit creatine kinase release from an isolated in-situ pig heart subjected to 1 h of normothermic regional ischemia followed by 1 h of global hypothermic arrest and 1 h of normothermic reperfusion. Preperfusion of the heart for 15 min prior to ischemic insult with 50 μM ibuprofen failed to mitigate the myocardial reperfusion injury. Ibuprofen, however, functioned as an anti-inflammatory agent, as judged by its ability to inhibit the influx of indium-111-labeled polymorphonuclear leukocytes and chromium-51 (51Cr)-labeled platelets into the ischemic and reperfused heart. It also blocked the cyclooxygenase pathway, as evidenced by the significant reduction of 6-keto-prostaglandin F1α and thromboxane B2 concentrations in the perfusate. Inhibition of cyclooxygenase resulted in increased accumulation of nonesterified fatty acids, particularly arachidonic acid, in the heart. These results suggest that although ibuprofen can inhibit polymorphonuclear leukocyte and platelet influx into the ischemic and reperfused heart, it causes further damage to the already ischemic heart by reducing prostacyclin concentration and increasing free fatty acids in the heart.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 87 (1992), S. 128-138 
    ISSN: 1435-1803
    Keywords: Heart ; stunning ; ischemia ; reperfusion ; infarctsize ; adaptation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of repetitive brief periods of coronary occlusion on subsequent prolonged ischemic insult was studied using a swine heart model. Four 5-min episodes of left anterior descending coronary artery (LAD) occlusion, each separated by 10 min of reperfusion, did not affect any of the regional or global myocardial functions examined, except that the level of adenosine triphosphate (ATP) dropped to some extent. Sixty minutes of LAD occlusion following four repeated stunnings further reduced the ATP level, but this reduction was significantly lower compared to nonstunned control. Myocardial global functions were not affected significantly by prolonged ischemic insult. Segment shortening (SS) was reduced comparably in both control and stunned groups. However, SS improved significantly during subsequent reperfusion in the stunned group compared to control. The experimental group also demonstrated reduced infarct size and an area of risk compared to nonstunned control. These results indicate that repeated stunning prior to irreversible ischemic insult can attenuate ischemic injury and post-ischemic dysfunction.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Bulletin of experimental biology and medicine 114 (1992), S. 1436-1439 
    ISSN: 1573-8221
    Keywords: erythrocytes ; ischemia ; myocardium ; gangliosides ; lipid peroxidation ; Na+, K+-ATPase ; lysophospholipids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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