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The Journal of Thoracic and Cardiovascular Surgery, Vol 84, 815-822, Copyright © 1982 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
H Feinberg, DS Rosenbaum, S Levitsky, NA Silverman, J Kohler and G LeBreton
Despite meticulous adherence to presently known principles of myocardial
preservation, reperfusion after aortic cross-clamping results in a unique
injury manifested by decreasing high-energy phosphate levels and increased
coronary resistance. We hypothesize that platelet deposition into the
coronary microvasculature is a major factor in reperfusion injury. To
differentiate platelet deposition due to subendocardial hemorrhage from
deposition due to vascular entrapment, we infused 111In-labeled platelets
together with 51Cr- labeled erythrocytes into 15 dogs that were on
normothermic bypass and subjected to 60 minutes of global ischemia followed
by 30 minutes of reperfusion. Platelet deposition is indicated only when
the proportion of platelets to erythrocytes in tissue exceeds that measured
by peripheral blood. Myocardial biopsy specimens were obtained after 10
minutes of bypass, 120 minutes of continuous bypass (Group I), and at the
end of reperfusion after global ischemia (Group II). In five dogs (Group
III), dipyridamole (1 mg/kg), an antiplatelet activation agent, was
administered in the preischemic period. Platelet deposition was expressed
as the number of radioactive-labeled platelets deposited per gram of
tissue. Bypass for 120 minutes resulted in only a minimal increase in
platelet deposition. However, normothermic ischemia followed by reperfusion
resulted in over a twofold increase in platelet deposition compared to
controls. Pretreatment with dipyridamole appeared to avoid platelet
deposition. These data indicate that platelet deposition in the coronary
microcirculation following surgically induced myocardial ischemia may be
associated with reperfusion injury and that antiplatelet drugs after this
sequence.
ARTICLES
Platelet deposition after surgically induced myocardial ischemia. An etiologic factor for reperfusion injury
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