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The Journal of Thoracic and Cardiovascular Surgery, Vol 97, 654-665, Copyright © 1989 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
MA Breda, DC Drinkwater, H Laks, S Bhuta, AF Corno, HG Davtyan and P Chang
Activated leukocytes release oxygen free radicals and cause microvascular
occlusion. This experiment tests the hypothesis that reperfusion with
leukocyte-depleted blood reduces injury after extended ischemic
preservation. An in vitro model consisting of an isolated, working neonatal
piglet heart and an adolescent support pig was used. Hearts were arrested
with a cold crystalloid cardioplegic solution, excised, and stored in 4
degrees C saline for 12 hours. Two groups were compared. In group 1 piglets
(n = 8), reperfused with whole blood, the maximum stroke work index was
0.91 +/- 0.29 x 10(3) erg/gm (mean +/- standard error of the mean). Group 2
piglets (n = 6), reperfused with blood depleted of leukocytes by a
polyester filter, had a maximum stroke work index of 11.6 +/- 1.0 x 10(3)
erg/gm. This difference was highly significant (p less than 0.0001). Group
1 exhibited severe injury with myofibrillar necrosis, mitochondrial
disruption, nuclear chromatin clumping, and moderate interstitial edema.
Group 2 had normal ultrastructure on electron microscopic examination. We
conclude that reperfusion with leukocyte-depleted blood prevents
reperfusion injury and results in excellent myocardial function after
long-term heart preservation.
ARTICLES
Prevention of reperfusion injury in the neonatal heart with leukocyte- depleted blood
University of California, Los Angeles 90024-1741.
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