Circulation, Vol 66, 397-400, Copyright © 1982 by American Heart Association
JC Mercier, U Lando, K Kanmatsuse, K Ninomiya, S Meerbaum, MC Fishbein, HJ Swan and W Ganz
Mechanical function remains depressed for hours and days after even brief
periods of ischemia. To determine whether the depressed function of the
reperfused myocardium could be improved y inotropic stimulation, we studied
segmental function during ischemia and after reperfusion using
mercury-in-Silastic length gauges in 15 dogs. During coronary artery
occlusion, segmental function could not be improved by inotropic
stimulation with dopamine. Release of occlusion after 30 minutes of
ischemia resulted in only slight improvement in segmental function
(systolic shortening at 20% of control). After reperfusion, segmental
function could be markedly enhanced by inotropic stimulation. The response
to inotropic stimulation was similar after reperfusion after 3 hours of
ischemia if the myocardium remained viable (nine dogs). When the myocardium
was necrotic (five dogs), there was no improvement after reperfusion,
either spontaneously or in response to inotropic stimulation. If applicable
to humans, these results suggest that intractable pump failure caused by
extensive but reversible ischemia could be effectively treated by
reperfusion and inotropic stimulation.
ARTICLES
Divergent effects of inotropic stimulation on the ischemic and severely depressed reperfused myocardium
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