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The Journal of Thoracic and Cardiovascular Surgery, Vol 95, 799-813, Copyright © 1988 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
DT Greenfield, LJ Greenfield and ML Hess
Oxygen-derived free radicals and intracellular calcium overload have been
implicated as mediators of myocardial ischemia/reperfusion injury. We
hypothesized that free radical scavengers or calcium channel blockers could
enhance the protection afforded the isolated, working rat heart by
crystalloid cardioplegia against this type of injury at 37 degrees C.
Hearts from 42 male rats in seven groups (n = 6) were studied in an
isolated, working heart preparation measuring aortic flow (ml/min/gm dry
wt), peak systolic pressure (mm Hg), coronary artery flow (ml/min/gm dry
wt), and calculated coronary vascular resistance (dyne.sec.cm-5/gm dry wt).
Creatine kinase and lactate dehydrogenase release were measured before
ischemia and at various times during the postischemic reperfusion period.
Time-matched control hearts (group 1) were perfused for 2 hours. After
finding that 30 minutes of ischemia and 10 minutes of reperfusion (group 2)
produced significant (p less than 0.01) functional impairment that was
completely protected (group 3) by a preischemic bolus of St. Thomas'
Hospital cardioplegic solution, we again found significant (p less than
0.01) functional impairment after 40 minutes of ischemia and 10 minutes
(group 4) or 20 minutes (group 5) of reperfusion despite a preischemic
bolus of St. Thomas' Hospital cardioplegic solution. Diltiazem (10 mg/L)
plus St. Thomas' Hospital cardioplegic solution (group 6) did not
significantly (p less than 0.01) enhance functional recovery. Addition of
superoxide dismutase plus catalase (200 microns/ml) (group 7) produced
marked improvement in functional recovery that did not differ significantly
(p less than 0.01) from control results (group 1). The creatine kinase and
lactate dehydrogenase data strongly supported the preceding functional
data. Coronary flow and vascular resistance were not significantly (p less
than 0.01) changed from control values in any group. We conclude that the
addition of superoxide dismutase and catalase but not diltiazem to St.
Thomas' Hospital cardioplegic solution can significantly enhance myocardial
protection against normothermic ischemia/reperfusion injury. This
implicates oxygen-derived free radicals as mediators of this type of
injury.
ARTICLES
Enhancement of crystalloid cardioplegic protection against global normothermic ischemia by superoxide dismutase plus catalase but not diltiazem in the isolated, working rat heart
Department of Medicine (Division of Cardiology), Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
This article has been cited by other articles:
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E. R. Rosenkranz Substrate Enhancement of Cardioplegic Solution: Experimental Studies and Clinical Evaluation Ann. Thorac. Surg., September 1, 1995; 60(3): 797 - 800. [Abstract] [Full Text] |
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