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  • 1
    Electronic Resource
    Electronic Resource
    The relationship between the perfusion deficit, infarct size and time after experimental coronary artery occlusion (1983)
    Springer
    Basic research in cardiology 78 (1983), S. 210-226 
    Details
    ISSN: 1435-1803
    Keywords: regional ischemia ; perfusion deficit, supply/demand ratio ; collateral flow ; instantaneous oxygen consumption ; development of necrosis ; infarct size
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is well known that coronary occlusions of short duration do not produce infarcts in the dog heart, but permanent occlusions always do. The aim of this paper was to investigate with quantitative direct measurements the determinants of infarct size within these two extremes. We measured left ventricular $$M\dot V_2$$ , coronary and collateral blood flow and infarct size after occlusion times varying between 45 minutes and 24 hours. $$M\dot VO_2$$ was kept low in one group by establishing low heart rates with a synthetic opiate. In another group, $$M\dot V_2$$ was kept elevated by giving synthetic catecholamines (dobutamine) that stimulated contractility and heart rate. Under the described experimental conditions LV-coronary blood flow reflected the true demand for blood and oxygen. The ratio of collateral blood flow over coronary blood flow (both measured with tracer microspheres) was therefore a good approximation of the supply-demand ratio (SD). Since collateral flow was inhomogeneously distributed across the left ventricular wall, the SD-ratio showed similar variations. As the collateral blood flow increased with elapsed time after coronary occlusion, the SD-ratio improved. Since high LV-O2-demand increased coronary flow but exerted practically no influence on collateral flow, this situation influenced the SD-ratio in a negative way. Decreased O2-demand had the opposite effect. The SD-ratio is thus a valid expression of the relative and absolute blood flow deficit as influenced by the local and general O2-demand. We found significant and characteristic correlations between the SD-ratio and infarct which was only influenced by time. A blood flow deficit of 90% (i.e., collateral flow =10% of required flow) produced a 50%-infarct (relative to the risk-region) with a 45-min occlusion but a 90%-infarct with occlusion times of 3 hrs and longer. If the perfusion deficit is only 0.5 (collateral flow =50% of required flow), no infarct is detectable at occlusion times shorter than 3 hrs. Small perfusion deficits of only 20% below required flow caused infarctions at 24 hrs and longer. In the group where the SD-ratio was closer to unity because of a low overall LV-O2-consumption (bradycardia), infarcts at t=24 hrs were significantly smaller than in the group with a high $$LV - M\dot VO_2$$ .
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01906674
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  • 2
    Electronic Resource
    Electronic Resource
    The effect of β-adrenergic blockade on infarct size following experimental coronary occlusion (1981)
    Springer
    Basic research in cardiology 76 (1981), S. 144-151 
    Details
    ISSN: 1435-1803
    Keywords: myocardial infarction ; β-adrenergic blockade ; infarct size ; collateral flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 10 Hunden wurde die Wirkung von Pindolol auf die Hämodynamik, die regionale Myokardperfusion und die Infarktgröße nach experimentellem Koronarverschluß untersucht. An jedem Herzen wurden hintereinander 2 mittelgroße Äste der linken Koronararterie okkludiert. Nach Ligatur (90 Minuten) und Reperfusion der ersten Arterie (Kontrollarterie) wurde die Inititaldosis Pindolol (0,25 mg/kg Körpergewicht) infundiert. Während der Ligatur (90 Minuten) der zweiten Arterie (Testarterie) wurde eine Erhaltungsdosis Pindolol (0,3 mg/kg Körpergewicht/90 Minuten) infundiert. Der linke Ventrikeldruck, LV-dp/dt max., Aortendruck und Herzfrequenz wurden kontinuierlich gemessen. Der myokardiale Sauerstoffverbrauch wurde vom Computer (Bretschneider-Formel) während des Experimentes berechnet. Die Myokarddurchblutung wurde mit Hilfe der “tracer microsphere”-Technik bestimmt. Das Nekrosegebiet wurde makrohistochemisch (NBT-Färbung) und das Perfusionsgebiet der verschlossenen Arterie wurde angiographisch definiert. Die resultierende Infarktgröße wurde als Quotient aus Nekrose-und Perfusionsgebiet in Prozent ausgedrückt. Pindolol verursachte einen signifikanten Abfall des linken Ventrikeldrucks, und LV-dp/dt, die Herzfrequenz, änderte sich nicht. Der myokardiale Sauerstoffverbrauch nahm signifikant von 7,9±1,4 auf 6,9±1,9 ml/min×100g ab. Der Kollateralfluß betrug im Perfusionsgebiet der Kontrollarterie 11,2±5,9% und in dem der Testarterie 10,0±4,4% der Normaldurchblutung. Die Infarktgröße konnte durch Pindolol nicht beeinflußt werden, sie betrug nach Verschluß der Kontrollarterie 48,2±22,2% und nach Verschluß der Testarterie 43,0±23,9%.
    Notes: Summary The effect of Pindolol on myocardial infarct size was studied in 10 open chest dogs. In each animal a sequential occlusion and reperfusion of 2 medium-sized branches of the left coronary artery was performed in the same heart. After occlusion and reperfusion of the control artery the initial dose of Pindolol (0.25 mg/kg body weight) was administered. Thereafter the test artery was occluded, followed by a maintenance dose of Pindolol (0.3 mg/kg body weight). The drug caused a significant decrease in LVP and LV-dp/dt but no change in heart rate. MVO2 also decreased significantly. Regional myocardial blood flow was measured with the tracer microsphere method. Collateral flow in the perfusion area of the control artery was 11.2±5.9% and in the area of the test artery 10.0±4.4% of normal. No change in the endo/epi ratio as a result of treatment was observed. The area of infarction (p-nitroblue tetrazolium-reaction) was divided by the area of perfusion (angiography). Infarct size, expressed as the percentage of the perfusion area. was 48.2±22.2% in the region of the control artery and 43.0±23.9% in the region of the test artery. The difference was statistically not significant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907953
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  • 3
    Electronic Resource
    Electronic Resource
    Ineffectiveness of methylprednisolone to reduce infarct size in experimental coronary occlusion (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 182-187 
    Details
    ISSN: 1435-1803
    Keywords: myocardial infarction ; collateral flow ; infarct size ; methylprednisolone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 10 Hunden wurde die Wirkung von Methylprednisolon auf die Myokarddurchblutung und die resultierende Infarktgröße nach experimentellem Koronarverschluß untersucht. An jedem Herzen wurden hintereinander zwei mittelgroße Äste der linken Koronararterie für 90 min okkludiert und anschließend reperfundiert. Der Verschluß der 1. Arterie erfolgte unter Kontrollbedingungen, es resultierte der Kontrollinfarkt. Vor dem Verschluß der 2. Arterie wurde Methylprednisolon (50 mg/kg Körpergewicht i.v.) injiziert, es resultierte der Testinfarkt. Die hämodynamischen Parameter (LVP, LV-dp/dt, AOP, HR) wurden kontinuierlich registriert, der myokardiale Sauerstoffverbrauch wurde vom Computer mit Hilfe der Bretschneider-Formel kalkuliert. Die myokardiale Durchblutung wurde mit Hilfe der “Tracer microsphere”-Technik bestimmt. Das Gebiet der myokardialen Nekrose wurde mit Hilfe der p-NBT-Färbung definiert, das Perfusionsgebiet wurde mit Hilfe der Post-mortem-Angiographie bestimmt Die Infarktgröße wurde als Quotient aus Nekrose- und Perfusionsgebiet in Prozent ausgedrückt. Die hämodynamischen Bedingungen waren in beiden Verschlußperioden vergleichbar, der Kollateralfluß betrug im Gebiet der Kontrollarterie 13,9±6,2% und im Gebiet der Testarterie 14,5±7,8% der Normaldurchblutung. Die resultierenden Infarktgrößen waren ohne Unterschied, der Kontrollinfarkt betrug 51±22%, der Testinfarkt 48±25%. Durch Methylprednisolon konnte weder der Kollateralfluß noch die resultierende Infarktgröße nach Koronarligatur beeinflußt werden.
    Notes: Summary Two medium-sized branches of the left coronary artery were prepared in each of 10 anesthetized open chest dogs for later occlusion. The first artery was occluded during 90 minutes and reperfused thereafter. This occlusion produced the control infarct. Methylprednisolone (50 mg/kg i.v.) was injected, and the second artery was occluded also for 90 minutes and reperfused thereafter. Both infarcts were made visible by staining left ventricular rings with p-nitrobluetetrazolium. Infarct size was compared with the size of the perfusion area, which we obtained from the postmortem angiogram. Both infarcts were equal in size and comprised 50% of the area of perfusion of the occluded artery. Methylprednisolone in a single high dose given prophylactically did not influence infarct size nor any of the measured parameters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908171
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of myocardial oxygen consumption on infarct size in experimental coronary artery occlusion (1982)
    Springer
    Basic research in cardiology 77 (1982), S. 170-181 
    Details
    ISSN: 1435-1803
    Keywords: infarct size ; myocardial oxygen consumption ; collateral flow ; oxprenolol ; dobutamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der Einfluß des kardialen Sauerstoffverbrauchs (MVO2) auf die Infarktgröße wurde bei 12 narkotisierten Hunden untersucht. Zwei voneinander völlig getrennte Seitenäste der linken Koronararterie wurde nacheinander am selben Herzen verschlossen. Das erste Gefäßkollektiv wurde bei einem MVO2 von 21,6±3,0 ml ·min−1. 100 g−1 okkuldiert, das zweite bei einem MVO2 von 5,9±1,5ml·min−1 ·100g−1. Die Infarktgröße, ausgedrückt als Fraktion des Perfusionsgebietes, war 43±28% in Gruppe 1 und 11±11% in Gruppe 2 (p〈0,005). Die Perfusionsgebiete, die okkludiert wurden, waren in beiden Gruppen gleich (17±4g, 19±6 g). Die Infarktgröße, die nach einer 90-min-Okklusion vom akuten Kollateralfluß abhängt, war in jedem Fall größer bei einem höheren MVO2. Somit kann ein, niedrigerer MVO2 zum Zeitpunkt des Verschlusses die Entwicklung der Nekrose zumindest hinauszögern.
    Notes: Summary The influence of myocardial oxygen consumption (MVO2) at the moment of coronary occlusion on the size of the ensuing necrosis was investigated in 12 anaesthetised dogs. A two-infarction model was used with a sequential occlusion of two distant coronary branches in the same heart, however under different levels of MVO2. One group of occlusions was produced at a high MVO2 of 21.6±3.0 ml O2... min−1. 100 g−1. This group was compared with a second in which necrosis proceeded at a low MVO2 estimated to be 5.9±1.5 ml O2·min−1. 100 g−1 averaged over a 90-min occlusion period. Infarct size expressed as percentage of perfusion area was 43±28% in group 1 and 11±11% in group 2 (p〈0.005). The mass of the perfusion area was equal in both groups (17±4 g, 19±6 g). The amount of myocardial necrosis, which after a 90-min occlusion depends on the acute collateral blood flow, was in every case greater under high MVO2. Thus a low MVO2 at the moment of occlusion can postpone myocardial necrosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908170
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  • 5
    Electronic Resource
    Electronic Resource
    Mitochondrial damage during myocardial ischemia (1984)
    Springer
    Basic research in cardiology 79 (1984), S. 207-217 
    Details
    ISSN: 1435-1803
    Keywords: ischemia ; reperfusion ; adenine ; pyridine ; mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of 3 hours of ischemia and 1 hour of reperfusion on biochemical, physiological and ultrastructural parameters were studied in 12 dogs. In the ischemic subendocardium without reperfusion, mitochondrial losses of adenine (ATP+ADP+AMP) and pyridine (NAD+NADH) nucleotides far exceeded those observed in whole tissue. Adenine nucleotide translocator (aNT) was severely inhibited and seemed to, be a sensitive indicator of a lesion of the inner mitochondrial membrane. Postischemic reperfusion led to a slight loss of adenine and pyridine nucleotides from the reversibly damaged subepicardium and to an enorous loss from the irreversibly damaged subendocardium. The washout of nucleotides from irreversibly damaged areas caused the negative para-Nitro Blue Tetrazolium (pNBT) staining of the infarcted tissue. Diagnosis of cell death with pNBT failed after the occlusion period without reflow because pyridine, although lost from the mitochondria, was still present in the tissue. In reversibly injured areas, mitochondrial function and ultrastructure were restored after reperfusion, although a significant nucleotide loss was found in the tissue. These studies suggest that mitochondrial ultrastructure and function may play a key role in cellular viability during recovery from ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908307
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  • 6
    Electronic Resource
    Electronic Resource
    Relation between lipolysis and glycolysis during ischemia in the isolated rat heart (1986)
    Springer
    Basic research in cardiology 81 (1986), S. 454-464 
    Details
    ISSN: 1435-1803
    Keywords: lipolysis ; ischemia ; glycerol-3-phosphate ; triglycerides ; reesterification ; isolated rat heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relation between lipolysis and glycolysis during ischemia was investigated in isolated perfused rat hearts. In hearts perfused with 11 mM glucose, ischemia caused a marked increase of glycerol release from 10 to 33 nmol/g wt weight/min. Substrate-free perfusion induced an initial stimulation of glycerol release, but lipolysis was subsequently reduced to values comparable to normoxic conditions. Neither did perfusion in the presence of acetate (10 mM) and β-hydroxybutyrate (10 mM) stimulate lipolysis. Inhibition of glycolysis by pyruvate prevented the increase of glycerol release during ischemia. These data suggest a tight link between glycolysis and lipolysis during ischemia which is probably mediated by the availability of glycolytically produced glycerol-3-phosphate for reesterification. In the absence of glycerol-3-phosphate, the lipolysis is regulated by product inhibition. As a consequence, the tissue triglyceride levels after perfusion remained fairly constant in all groups of hearts. The calculated energy loss by the reesterification cycle during ischemia was found to be approximately 2.5% of the total energy production. These data are inconsistent with the assumption that this energy loss contributes significantly to the negative energetic balance of the heart during ischemia. Removal of fatty acids by reesterification may constitute a protective mechanism in order to prevent excessive intracellular accumulation of fatty acids and derivative esters during ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907751
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