AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 637-H643, Copyright © 1985 by American Physiological Society
Superoxide dismutase enhances recovery following myocardial ischemia
K. P. Burton
Oxygen-derived free radicals, specifically superoxide (O-2) and the
hydroxyl radical (OH.), have been implicated as possible mediators in the
development of myocardial damage induced by ischemia and reflow. The
purpose of this study was to examine the ability of superoxide dismutase
(SOD), a O-2 scavenging enzyme, to protect the heart against functional and
structural alterations due to ischemia and reflow. An isolated perfused
rabbit interventricular septal preparation was used for these experiments.
Septa were treated with SOD by adding either 10 or 20 micrograms/ml of the
enzyme to the perfusion solution 15 min prior to ischemia and during
reflow. Other septa were not treated. Septa were made ischemic for 1 h and
reperfused for 1 h. The contractile performance of reperfused septa was
found to be significantly improved in SOD-treated septa when compared with
nontreated septa. After 60 min of reflow, values for nontreated, 10- and
20-micrograms/ml SOD-treated septa, respectively, were 48.5 +/- 5.2 (SE),
67.4 +/- 4.2, and 82.0 +/- 3.8% of control values for developed tension.
The rise in resting tension observed with reflow was significantly
decreased. SOD treatment also provided significant protection of myocardial
ultrastructure. The percent of myocytes showing normal structure was
increased approximately 40%, and the percentages of myocytes showing mild
or severe damage were decreased approximately 30 and 15%, respectively, for
SOD-treated septa. Vessel structure showed a similar trend. Thus SOD
preserves myocardial function and structure in septa reperfused following
ischemia. These results support the possibility that oxygen-derived free
radicals may be involved in the damage resulting from ischemia and reflow.
