Myocardial energetics

experimental and clinical studies to address its determinants and aerobic limit

Karl Weber, J. S. Janicki, P. Sundram

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The major determinants of myocardial oxygen consumption (M {Mathematical expression}O2) were examined in the isolated, servo-regulated, canine heart in which coronary perfusion pressure, heart rate, ventricular volume and pressure could be individually monitored and controlled. We found that the integral of systolic wall force and the time derivative of systolic force development were major determinants of M {Mathematical expression}O2. Net M {Mathematical expression}O2, seen in response to increments in contractility (dobutamine) and heart rate, were the result of the relative increments in each of these determinants. Additional studies were performed to assess the heart's metabolic reserve and aerobic limit (i.e., before the onset of lactate production). We found that with increments in left ventricular work, mediated by increments in filling volume, heart rate, and contractility (dobutamine), myocardial lactate production could be induced, but was dependent on the level of coronary perfusion pressure. When the aerobic limit of the myocardium was exceeded, its performance declined and pulsus alternans appeared. In patients with cardiomegaly and advanced heart failure given the phosphodiesterase inhibitors enoximone and piroximone we did not observe a rise in M {Mathematical expression}O2 or the appearance of lactate production in the majority of patients. When patients with documented idiopathic (dilated) cardiomyopathy and marked heart failure received hemodynamically significant doses of dobutamine alone or in combination with amrinone, there again was no evidence of lactate production or a rise in M {Mathematical expression}O2, while a marked improvement in ventricular function was noted. Thus, these agents served to improve the efficiency of the dilated failing heart. Hence we would conclude that in most cases, the dilated failing heart has an adequate metabolic reserve. Its performance, and indeed its efficiency, can be improved with pharmacologic agents having positive inotropic properties without adversely altering myocardial energetics.

Original languageEnglish (US)
Pages (from-to)236-246
Number of pages11
JournalBasic research in cardiology
Volume84
Issue number1
DOIs
StatePublished - Dec 1 1989

Fingerprint

Dobutamine
Lactic Acid
piroximone
Heart Rate
Enoximone
Heart Failure
Perfusion
Amrinone
Myocardial Contraction
Pressure
Phosphodiesterase Inhibitors
Ventricular Function
Dilated Cardiomyopathy
Cardiomegaly
Ventricular Pressure
Oxygen Consumption
Pulse
Canidae
Myocardium
Clinical Studies

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Myocardial energetics : experimental and clinical studies to address its determinants and aerobic limit. / Weber, Karl; Janicki, J. S.; Sundram, P.

In: Basic research in cardiology, Vol. 84, No. 1, 01.12.1989, p. 236-246.

Research output: Contribution to journalArticle

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