AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 681-H687, Copyright © 1989 by American Physiological Society
Deleterious effect of ouabain on myocardial function during hypoxia
M. J. Cunningham, C. S. Apstein, E. O. Weinberg and B. H. Lorell
Cardiac Muscle Research Laboratory, Cardiovascular Institute of Boston University School of Medicine, Massachusetts.
The effect of cardiac glycosides on myocardial function during hypoxia is
controversial. Accordingly, we studied left ventricular performance during
hypoxia and reoxygenation in the presence of a mildly inotropic, nontoxic
dose of ouabain using isolated, isovolumic, buffer-perfused rabbit hearts.
After 15 min of hypoxia, left ventricular developed pressure was less in
the ouabain-treated group than in controls (35 +/- 4 vs. 55 +/- 3 mmHg, P
less than 0.025). Left ventricular end-diastolic pressure (LVEDP) increased
more during hypoxia in the presence of ouabain (9 +/- 1 to 32 +/- 7 with
ouabain vs. 9 +/- 1 to 14 +/- 3 mmHg without ouabain, P less than 0.005)
despite comparable degrees of coronary vasodilatation and myocardial
lactate production in the two groups. When coronary flow was abruptly
reduced to zero to eliminate the coronary turgor contribution to diastolic
pressure, LVEDP after 15 min of hypoxia in the presence of ouabain was
greater than that in control hearts that did not receive ouabain (13 +/- 4
vs. 4 +/- 1 mmHg, P less than 0.05), implicating greater diastolic
myocardial fiber tension in the ouabain group during hypoxia. With
reoxygenation, recovery of developed pressure was less and end-diastolic
pressure remained elevated in the ouabain-treated group when compared with
controls. We conclude that a modestly inotropic dose of ouabain exacerbates
the decrease in diastolic ventricular distensibility induced by hypoxia,
worsens the decline in developed pressure during hypoxia, and impairs
recovery during reoxygenation.
