Zusammenfassung
Es wurden zwölf Versuche an gesunden, narkotisierten und konstant ventilierten Hunden durchgeführt. Blutdruck, Säure-Basenhaushalt, Sauerstoffversorgung und Lactat/Pyruvat-Stoffwechsel wurden mittels Blutanalysen verfolgt. Die Aktivitäten von neun glykolytischen Enzymen wurden im linksventrikulären Myokard gemessen. Mit der Reservoir-Technik wurde ein vermutlich irreversibler hämorrhagischer Schock erzeugt und seine metabolischen Auswirkungen auf die Blutparameter registriert. Die Analyse des coronarvenösen Blutes ergab keine Anhaltspunkte für einen Sauerstoffmangel des Herzens. Die Enzymaktivitäten waren nach dem Schock mehrheitlich erhöht. Ausnahmen bildeten Pyruvatkinase, LDH und α-HB-DH. Zwischen den Entnahmestellen traten vor allem in der Innenschicht Aktivitätsgradienten zutage. Das im Normalzustand gefundene Muster der transmuralen Aktivitätsgradienten war nach dem Schock gestört. Die Befunde sprechen gegen einen Sauerstoffmangel als Ursache des Herzversagens im Schock. Sie lassen sich als funktionelle Folgen von Strukturveränderungen interpretieren, die mit Wirkungen der Katecholamine oder mit toxischen Substanzen aus der Peripherie zusammenhängen könnten.
Summary
Twelve experiments were performed on healthy, anesthetized dogs on constant ventilation. Blood pressure, acid-base status, oxygen supply and lactate/pyruvate metabolism were monitored in the blood. The activities of nine glycolytic enzymes were assayed in left ventricular myocardium. A presumably irreversible state of hemorrhagic shock was produced by the reservoir technique and its metabolic sequels recorded in the blood. The analysis of coronary sinus blood did not reveal an oxygen deficit of the heart. The majority of the enzymes assayed showed higher activities following shock. Exceptions were pyruvate kinase, LDH and α-HB-DH. Activity differences between sampling sites appeared following shock especially in the inner layer of the left ventricle. The pattern of transmural activity gradients previously found in the normal state was disturbed. The findings are against an oxygen deficit as a cause of cardiac deterioration in shock, suggesting structural derangements possibly due to catecholamine effects or toxic substances of peripheral origin.
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Work supported by Research Grant No. 4139 from the Swiss National Foundation for the Advancement of Scientific Research.
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Lundsgaard-Hansen, P., Meyer, C., Riedwyl, H. et al. Transmural gradients of glycolytic enzyme activities in left ventricular myocardium. Pflügers Arch 301, 144–161 (1968). https://doi.org/10.1007/BF00362732
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DOI: https://doi.org/10.1007/BF00362732