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  • 1
    ISSN: 1432-2307
    Keywords: Myocardial infarction ; Tetrazolium salts ; NAD ; Oxidoreductases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tetrazolium salts (NBT) stain normal myocardium whereas infarcts are not stained. We tried to elucidate the staining mechanism which discriminates normal from infarcted canine myocardium. The left anterior descending coronary artery (LAD) was occluded in dogs for between 4 and 32 h. The activities of four different tissue dehydrogenases were measured after 4, 8, 16, and 32 h of ischaemia. Nicotinamide adenine dinucleotides (NAD, NADH, NADPH) were determined in needle biopsies taken from the ischaemic region 1/2, 1, 11/2, 2 and 4 h after occlusion of the LAD. In another set of experiments the NBT stain was altered by the addition of NADH, NAD, NADPH, NADP, succinate, lactate and phenazine methosulfate respectively and the effect of the added substances on the previously nonstained infarcts was examined. We further compared histochemically determined infarct size to the ultrastructural extent of infarcts. Activities of the tissue dehydrogenases did not change after 4 h of ischaemia, although the NBT stain revealed a large infarction. At that time total NAD, the sum of NAD+NADH, had decreased from about 600 pmoles/mg tissue to about 200 pmoles/mg tissue and addition of the coenzymes or succinate could “repair” the biochemical lesion. After 24 h of ischaemia the activities of dehydrogenases and diaphorases were markedly decreased. Our data indicate that loss of the reduced coenzymes plays a key role in identifying myocardial infarction with tetrazolium salts. In older infarctions loss of coenzymes is joined by decreased activities of dehydrogenases and diaphorases. The principal mechanisms of staining is an enzymatic cycling.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: collaterals ; myocardial protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous work of this laboratory has shown that collateral flow can be increased over six weeks by a subcritical external constriction of the circumflex artery causing a 50±10% reduction of postocclusive reactive hyperemia. To investigate collateral function in acuté myocardial infarction, the model was used to ligate two distant coronary branches on the ventricle simultaneously in order to compare in 8 dogs infarct size and perfusion area of the ligated vessels in control and collateralized sections. The acute collateral flow measured 7.2±2.5 ml/100 g/min−1 and increased to 17.3±6.7 (p〈0.001) over 6 weeks. Separate analysis revealed a predominant increase of collateral flow in the epicardial layers 23.1±7.5 (p〈0.01) versus 6.9±2.8 (p〈0.01) in the subendocardium. Infarct size in the control area was 52.0±14.7% of the perfusion area, in the collateralized zone 19.0±14.2% (p〈0.001). Infarct size expressed as per cent of perfusion area and collateral flow in the area at risk expressed as per cent of flow of normal sections correlated: (r=0.76; p〈0.05). Therefore, infarct size after a 6 hour coronary occlusion can be considered a function of the collateral flow over normal perfusion ratio. Localized induction of collaterals in this model caused a significant reduction of infarct size in relation to the perfusion area at risk.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1803
    Keywords: collateral development ; experimental model ; fixed coronary constriction ; subcritical stenosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Ein Hundemodell zur standardisierten Induktion von Kollateralen mit Hilfe eines externen Konstriktors wird vorgestellt, bei welchem eine Okklusion der Koronararterie nicht vorgesehen ist und wenigstens über 6 Wochen die Myokardperfusion in Ruhe nicht eingeschränkt wird. Flußmessungen wurden mit einem elektromagnetischen Flowmeter und mit radioaktiven Mikrosphären im akuten Versuch durchgeführt und nach 6 Wochen wiederholt. Die Ergebnisse zeigten eine Zunahme des Kollateralflusses von 21,2±11,8 ml/100g/min−1 auf 42,8±16,2 ml/100 g/min−1 (p〈0.05). Die regionale Durchblutung wies einen transmyokardialen Gradienten auf, welcher die subepikardialen Schichten gegenüber den subendokardialen bevorzugt: 49,3±25 ml/100 g/min−1 gegenüber 33,1±17,3 ml/100 g/min−1 (p〈0,05). Die mit dem Flowmeter gemessene reaktive Hyperämie nahm über 6 Wochen um 21% ab, bedingt durch eine Verengung der Stenosen aufgrund von Intimareaktionen im Konstriktorbereich, während die mit Mikrosphären gemessene Durchblutung aufgrund zusätzlicher Kollateralversorgung um 9% zunahm.
    Notes: Summary A canine model for a standardized induction of collaterals is presented with a fixed external constrictor that is not designed to induce an occlusion of the coronary artery and at least over the timespan of 6 weeks does not impair perfusion under resting conditions in the myocardium-at-risk. The coronary constriction was standardized by a reduction of the postocclusive reactive hyperemia of 50%. Flow measurements were performed by flowmeter and by radioactive microspheres acutely and after an interval of 6 weeks of constriction. The results showed an increase of the collateral flow from 21.2±11.8 ml/100g/min−1 to 42.8±16.2 ml/100g/min−1 (p〈0.05). The regional perfusion exhibited a transmyocardial gradient in favour of the subepicardial layers with 49.3±25 ml/100g/min−1 as compared to 33.1±17.3 ml/100g/min−1 (p〈0.05) of the endocardial layers. Reactive hyperemia, as determined by flowmeter, was decreased by 21% after 6 weeks on account of slow progression of the coronary constriction due to intimal reactions, whereas reactive hyperemia, as determined by the microsphere method, increased by 9% due to additional collateral channels.
    Type of Medium: Electronic Resource
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