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Alterations of mitochondrial function as detected in left ventricular myocardium of rats with acute aortic constriction

Änderungen der Mitochondrienfunktion im linksventrikulären Myokard der Ratte bei akuter Aortenkonstriktion

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Summary

Respiratory activity of the left ventricle of isolated perfused heart from rats with severe aortic constriction was examined by means of optical recording of intracellular redox changes. The speed of state-5-to-state-3 transition (recovery from short period of anoxia) was monitored fluorimetrically (PdN) and spectrophotometrically (cyt aa3).

Three days after stenosis of the abdominal aorta, the reoxidation of PdN was significantly accelerated, while the amplitude of the anoxic signal was rather comparable to that of control hearts. One week later, the rate of reduced NADH removal was considerably depressed.

Zusammenfassung

Die respiratorische Aktivität des linken Ventrikels beim isoliert-perfundierten Rattenherzen mit schwerer Aortenkonstriktion wurde durch optische Registrierung der intrazellulären Redoxänderungen untersucht. Die Geschwindigkeit des Übergangs vom Status 5 zum Status 3 (Erholung von kurzen Anoxieperioden) wurde fluorimetrisch (PdN) und spektrophotometrisch (cyt aa3) untersucht.

3 Tage nach Stenosierung der abdominalen Aorta war die Reoxidation der PdN signifikant beschleunigt, während die Amplitude des anoxischen Signals weitgehend der des Kontrollherzens vergleichbar waren. Eine Woche später war die Geschwindigkeit der NADH-Reoxidation beträchtlich vermindert.

Die Änderungen in der Fähigkeit der Mitochondrien, einen Überschuß an NADH zu oxidieren, scheint nicht mit einer veränderten Sauerstoffverfügbarkeit in Beziehung zu stehen, da sowohl die Geschwindigkeit der cyt-aa-3 Reoxidation und der Geschwindigkeit der Mb-Reoxigenation bei Vergleich der verschiedenen Gruppen bemerkenswert konstant war. Diese Änderungen reflektieren wahrscheinlich Veränderungen in der Organisation der respiratorischen Einheiten als solcher, oder sie sind Folge veränderter transmembranärer Translokationen, die bei der Kontrolle der Atmung beteiligt sind. Wie immer der wahre Mechanismus des beobachteten Phänomens beschaffen ist, so lassen die Ergebnisse auf jeden Fall eine Hemmung der Atmungskette am Ende der ersten Woche druckinduzierter Überbelastung vermuten.

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Moravec, J., Renault, G. & Hatt, P.Y. Alterations of mitochondrial function as detected in left ventricular myocardium of rats with acute aortic constriction. Basic Res Cardiol 73, 535–550 (1978). https://doi.org/10.1007/BF01906792

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