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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 79 (1984), S. 440-447 
    ISSN: 1435-1803
    Keywords: myocardium ; ischemia ; infarction ; reperfusion ; pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the temporal and spatial development of infarcts in porcine hearts to evaluate the time-dependent beneficial effect of reperfusion on infarct size. The left anterior descending coronary artery (LAD) was occluded in 17 pigs for different periods of time followed by 4 hours of reperfusion. Transmural needle biopsies subdivided into subendocardial and subepicardial halves were taken from the ischemic apex after 60 min of ischemia to determine the tissue concentrations of ATP and NAD. The myocardium-at-risk was assessed with a fluorescent dye injected into the right atrium at the end of the experiments, just after the LAD had been reoccluded. The excised hearts were cut into slices parallel to the heart basis. The ischemic myocardium was measured by planimetry of the nonfluorescent areas whereas the infarcted tissue was determined with the NBT stain and related to the area-at-risk. Ischemic cell death started in the jeopardized left ventricular subendocardial septum after about 30 min of ischemia. The further progress involved the right subendocardial septum and the subendocardium of the left anterior free wall. Already after 75 min of ischemia most of the myocytes-at-risk were irreversibly injured. Infarctions reached their final extent after 90–120 min of ischemia. These results indicate that in hearts without a significant collateral blood flow reperfusion can only reduce infarct size if its initiated within 60–75 min of ischemia. Like in canine hearts infarctions progress from the ischemic subendocardium towards the outer layers.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: mannitol ; ischemia ; reperfusion ; infarct size ; pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the effect of reperfusion with hyperosmotic mannitol on the infarct size in porcine hearts. The distal half of the left anterior descending coronary artery was occluded in each of 21 anesthetized pigs for 75 min and was reperfused for 2 h. During reperfusion mannitol (1075 mosmol/kg) was intracoronarily infused at a dose of 0.5 ml/min in 6 pigs (“low” mannitol group), at a dose of 1.5 ml/min in another 6 pigs (“high” mannitol group), and at a dose of 5 ml/min in 3 pigs for the first 8 min of reperfusion (“very high” mannitol group). 6 pigs served as controls. Although mannitol infusion increased plasma osmolality in the ischemic, reperfused myocardium in all experiments, the infarct size expressed as the ratio of the infarcted tissue over the area at risk of necrosis was not significantly influenced. Infarct size amounted to 72±25% in the control group, to 75±14% in the “low” mannitol group, to 78±18% in the “high” mannitol group, and to 93±8% in the “very high” mannitol group. These results clearly indicate that reperfusion with hyperosmotic mannitol after 75 min of ischemia does not exert any beneficial effect on the infarct size.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1803
    Keywords: ischemia ; reperfusion ; vitamin E ; infarct size ; regionalsystolic shortening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty pigs were randomly assigned to a blind treatment with vitamin E or placebo. Ten animals each received 0.5g d-alpha tocopherol intravenously before ischemia (group 1) or before reperfusion (group 2). Ten control pigs were treated with a lipid emulsion as placebo. The left anterior descending coronary artery was distally ligated for 45 min followed by 3 days of reperfusion. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Myocardial and plasma concentrations of vitamin E were determined by high-performance liquid chromatography. Global hemodynamic parameters and estimated left ventricular oxygen consumption did not differ among the three groups. Intravenous treatment with vitamin E raised the plasma levels of this vitamin from 1 ± 0.3 mg/l (control group) to 21 ± 6 mg/l before ischemia, to 4 ± 2 mg/l before reperfusion and to 2 ± 0.6 mg/l at the end of the experiments in group 1. In group 2, vitamin E plasma levels increased from 1 ± 0.3 mg/l to 24 ± 13 mg/l before reperfusion and to 2 ± 0.6 mg/l after 3 days of reperfusion. At the end of the experiments, myocardial vitamin E concentrations amounted to 4.2 ± 0.7 ng/mg fresh weight (control group), 9.7 ± 2.1 ng/mg (group 1), and to 8.7 ± 1.4 ng/mg (group 2). The increase in vitamin E plasma concentration was not associated with a cardioprotective effect. Infarct sizes of the three groups (group 1: 68 ± 12%, group 2: 66 ± 15%, control group: 69 ± 8%) were almost identical. Furthermore, recovery of systolic shortening was not improved by the acute vitamin E treatment. Mean systolic shortening of the reperfused segment amounted to 4% in the two treatment groups and 3% in the control group after 3 days of reperfusion. These results suggest that an acute increase in vitamin E plasma concentration before ischemia or during the early phase of reperfusion does not protect the ischemic, reperfused porcine heart.
    Type of Medium: Electronic Resource
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