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February 1, 1965American Journal of Physiology-Legacy Content149 citations

Myocardial reactive hyperemia in the unanesthetized dog

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RORay A. OlssonForschungszentrum JülichDGDonald E. GreggWalter Reed Army Institute of Research

Key Result

Coronary occlusion in unanesthetized dogs resulted in an overpayment of flow debt during reactive hyperemia averaging 500 ± 200%, driven independently by occlusion duration and control flow rate.

Key Points

  • The study examines how different factors influence myocardial reactive hyperemia after coronary artery occlusion.
  • Implanted electromagnetic flowmeters on coronary artery branches of 5-24 day old dogs.
  • Measured duration of occlusion and control flow rates as determinants of reactive hyperemia flow.
  • Analyzed phasic coronary flow curves to assess changes in systolic and diastolic flows.
  • Flow debt averaged 500 ± 200%, indicating that myocardial flow is often compensated after occlusion.
  • Systolic flow increased during reactive hyperemia due to a decrease in myocardial contractility.
  • Reactive hyperemia was associated with the accumulation of vasodilator metabolites during occlusion.

Structured PICO

P
Population
Unanesthetized dogs 5–24 days after the implantation of electromagnetic flowmeters on coronary artery branches
I
Intervention
Coronary occlusion
C
Comparator
Control flow rate
O
Outcome
Volume of reactive hyperemia flowsurrogate

Myocardial reactive hyperemia following coronary occlusion in unanesthetized dogs results in a massive overpayment of flow debt, averaging 500%, driven by increases in both systolic and diastolic flow.

Abstract

Studies of myocardial reactive hyperemia in dogs 5–24 days after the implantation of electromagnetic flowmeters on coronary artery branches reveal that the duration of occlusion and the control flow rate are independent determinants of the volume of reactive hyperemia flow. Flow debt is almost always overpaid, the average figure being 500 ± 200%. Phasic coronary flow curves show an increase in both systolic and diastolic flow during reactive hyperemia, the increase in systolic flow being due in part to decreased myocardial contractility. Myocardial reactive hyperemia is thought to be due to the accumulation of vasodilator metabolites during the period of coronary occlusion.

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Cite This Study

Olsson et al. (1965) studied Myocardial reactive hyperemia. Coronary occlusion was evaluated on Volume of reactive hyperemia flow. Coronary occlusion in unanesthetized dogs resulted in an overpayment of flow debt during reactive hyperemia averaging 500 ± 200%, driven independently by occlusion duration and control flow rate.

synapsesocial.com/papers/6a0d642748a82a5ce309b6d7https://doi.org/10.1152/ajplegacy.1965.208.2.224
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