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The Journal of Thoracic and Cardiovascular Surgery, Vol 95, 960-968, Copyright © 1988 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Reperfusion injury after temporary coronary occlusion

J Vinten-Johansen, WE Johnston, SA Mills, KB Faust, KR Geisinger, RJ DeMasi and AR Cordell
Department of Surgery, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, N.C. 27103.

In 24 anesthetized open-chest dogs, we examined the time course of changes in contractile function, diastolic muscle stiffness (sonomicrometry), tissue water content, and ultrastructure after 1 hour of occlusion of the left anterior descending coronary artery and after 2 hours of unmodified reperfusion. One hour of occlusion of the left anterior descending artery replaced active shortening with passive bulging (21.4% +/- 2.9% versus -5.9% +/- 0.9%, p less than 0.05) in the involved segment. There was no increase in either subendocardial water content (78.6% +/- 0.1% versus 79.7% +/- 0.7%) or operative muscle stiffness (2.80 +/- 0.72 versus 2.36 +/- 0.42 mm Hg/mm) after the occlusion period. There were only mild to moderate ultrastructural alterations suggestive of reversible injury. In sharp contrast, reperfusion was associated with a 2.48% increase in subendocardial water content (p less than 0.05), a 42% increase in diastolic muscle stiffness (3.34 +/- 0.42 mm Hg/mm, p less than 0.05), and greater ultrastructural damage. We conclude that myocardial injury is significantly extended with unmodified blood reperfusion after temporary coronary occlusion.

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