Basic Research in Cardiology

, Volume 78, Issue 1, pp 85–98 | Cite as

Effects of acute vagally-mediated bradycardia on systemic hemodynamics and coronary blood flow before and after coronary stenosis

  • J. Senges
  • I. Rizos
  • U. Mittmann
  • J. Brachmann
  • L. Beck
  • D. Opherk
  • H. -D. Hammann
  • E. Mayer
  • W. Kübler
Original Contributions

Summary

The effects of short episodes (1 min) of vagally-mediated bradycardia were studied in 9 anesthetized dogs utilizing vagal stimulation and slow atrial pacing (120 and 80 beats/min) before and after graded coronary constriction of the left anterior descending (LAD) and the left circumflex (CCA). In the presence of 90% LAD stenosis, bradycardia tended to restore both the elevated total LAD coronary vascular resistance (CVR-LAD) and the reduced, total CVR-CCA towards control levels obtained at corresponding slow rates in the absence of coronary stenosis; as a result, LAD coronary flow (F-LAD) was relatively less reduced and the accessory rise of F-CCA disappeared. In the presence of combination of 90% LAD plus 70% CCA stenosis, the effects of bradycardia on total CVR-LAD and F-LAD were similar to those obtained with single 90% LAD stenosis, but the accessory flow through the CCA was abolished resulting in no significant difference of the rate-dependent alterations of total CVR-CCA and F-CCA as compared with those observed in the absence of coronary stenosis. In the presence of single or combined coronary stenosis, bradycardia restored the depressed aortic pressure and cardiac output towards control values obtained at comparable slow rates before coronary stenosis. The results support the concept that in the presence of 90% LAD stenosis vagally-mediated bradycardia 1) decreases the tension-time index (myocardial nutritional demand) shifting cardiac performance to less expensive “flow work” and 2) facilitates antegrade flow through the highly stenotic LAD thereby inhibiting accessory flow through the nonstenotic CCA.

Key words

heart rate bradycardia coronary blood flow tension-time index coronary constriction 

Zusammenfassung

Die Wirkung kurzdauernder (1 min) vagusinduzierter Bradykardien wurde in 9 anästhesierten Hunden untersucht. Vor und nach abgestufter Koronarstenose des Ramus interventricularis anterior (LAD) und des Ramus circumflexus (CCA) der linken Koronararterie wurde vagal gereizt und atrial stimuliert (120 und 80/min). Bei Vorliegen einer 90%-LAD-Stenose bewirkte eine Bradykardie in der Tendenz eine Änderung des erhöhten LAD-Koronarwiderstands (CVR-LAD) und des reduzierten CVR-CCA zu den Kontrollwerten hin, die bei entsprechend langsamen Herzfrequenzen in Abwesenheit einer Koronarstenose ermittelt wurden. Daraus folgte, daß der LAD-Koronarfluß (F-LAD) relativ weniger abnahm und der sich daraus ergebende Anstieg des F-CCA verschwand. Bei gleichzeitigem Vorliegen einer 90%-LAD-und einer 70%-CCA-Stenose waren die Auswirkungen der Bradykardie ähnlich denjenigen, die bei einer einzelnen 90%-LAD-Stenose beobachtet wurden; dagegen war der zusätzliche Fluß durch die CCA aufgehoben. Daher bestand keine signifikante Differenz zwischen den frequenzabhängigen Änderungen des CVR-CCA und F-LAD im Vergleich zu den in Abwesenheit von Koronarstenosen beobachteten Änderungen. Bei Vorliegen einzelner oder kombinierter Koronarstenosen führt eine Bradykardie zu einer Umkehrung der Abnahme des Aortendrucks und des Herzminutenvolumens in Richtung der Kontrollwerte bei vergleichbar langsamen Frequenzen vor Koronarstenose. Die Ergebnisse unterstützen die Vorstellung, daß bei 90%-LAD-Stenose vagusinduzierte Bradykardie 1. den Spannungs-Zeit-Index (myokardialer Nährstoffbedarf) vermindert und damit die Herzleistung in Richtung Flußarbeit verschiebt und 2. den antegraden Fluß durch die hochgradig stenosierte LAD erleichtert und damit den zusätzlichen Fluß durch die nichtstenosierte CCA verhindert.

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Copyright information

© Dr. Dietrich Steinkopff Verlag 1983

Authors and Affiliations

  • J. Senges
    • 1
    • 2
  • I. Rizos
    • 1
    • 2
  • U. Mittmann
    • 1
    • 2
  • J. Brachmann
    • 1
    • 2
  • L. Beck
    • 1
    • 2
  • D. Opherk
    • 1
    • 2
  • H. -D. Hammann
    • 1
    • 2
  • E. Mayer
    • 1
    • 2
  • W. Kübler
    • 1
    • 2
  1. 1.Abteilung Innere Medizin III (Kardiologie) der Medizinischen UniversitätsklinikHeidelbergGermany
  2. 2.Abteilung Experimentelle Chirurgie der Chirurgischen UniversitätsklinikHeidelbergGermany

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